Melatonin and Cancer: 2026 Complete Integrative Oncology Guide
Use Melatonin for a Defined Goal With the Right Monitoring
Sleep support, circadian timing and investigational oncology use are different clinical questions. A physician can review dose, timing, medications, fall risk and active treatment.
- The goal, dose and timing are defined clearly
- Sedation, interactions and treatment context are reviewed
- Call now for an immediate response from our Patient Care Team
Speak With Our Patient Care Team
Share your diagnosis, sleep pattern, current treatment and melatonin dose or product.
- The goal, dose and timing are defined clearly
- Sedation, interactions and treatment context are reviewed
- Questions before scheduling are always welcome
Melatonin and cancer research extends far beyond sleep. Melatonin is a naturally produced indoleamine hormone with circadian, mitochondrial, metabolic, immune, antioxidant, pro-oxidant, anti-estrogenic, anti-angiogenic, anti-metastatic and cell-signaling effects that have been studied across a remarkably wide range of cancers.
At Sunridge Medical in Scottsdale, Arizona, melatonin may be considered as part of a physician-directed integrative cancer treatment program when appropriate for the individual patient. The clinical question is not simply whether melatonin helps someone sleep. The more interesting question is whether melatonin can influence tumor biology, treatment response, circadian signaling, mitochondrial function, cancer stem-cell behavior, inflammation and quality of life in ways that may complement a broader oncology strategy.
The research is unusually broad. Human studies include randomized trials in non-small cell lung cancer, breast cancer, metastatic colorectal cancer, glioblastoma, brain metastases and advanced solid tumors. Laboratory and animal research extends into triple-negative breast cancer, prostate cancer, cholangiocarcinoma, colorectal cancer, leukemia, osteosarcoma, melanoma and other tumor types.
The evidence is also mixed. Several older trials reported striking benefits, while larger or more modern studies have not always confirmed those findings. That makes melatonin one of the most interesting natural compounds in integrative oncology—and one that deserves careful, evidence-based discussion rather than either dismissal or overstatement.
Melatonin is a circadian signaling molecule with important research in sleep, mitochondrial biology and cancer treatment support.
RESEARCH OVERVIEW
Melatonin Is More Than a Sleep Hormone
Melatonin is synthesized primarily by the pineal gland during darkness and helps coordinate the body's circadian timing system. Its secretion normally rises in the evening, remains elevated during the biological night and falls toward morning.
In oncology, that circadian biology matters because cancer cells do not exist independently of the body's timing system. Hormone signaling, DNA repair, immune activity, oxidative metabolism, cell division and drug metabolism all show circadian organization.
Melatonin also acts through multiple biological routes. It can signal through membrane receptors—especially MT1 and MT2—and can exert receptor-independent effects inside cells. Breast-cancer research has demonstrated MT1 expression in human breast tumors and breast-cancer cell lines, supporting a direct receptor-mediated pathway for melatonin's growth-regulating effects.16
Melatonin's biological breadth is one reason it has been studied not only as a sleep aid, but as a potential oncostatic and treatment-supportive molecule.
RESEARCH OVERVIEW
Circadian Biology May Be Part of Cancer Biology
Cancer research increasingly recognizes that the timing environment surrounding a tumor matters.
Melatonin is the body's strongest hormonal signal of darkness. Exposure to light at night can suppress nocturnal melatonin and disrupt normal circadian signaling. Experimental breast-cancer research has shown that melatonin signaling can affect tumor metabolism, estrogen signaling, growth pathways and treatment response.
More recently, a randomized placebo-controlled study in night-shift workers found that melatonin supplementation increased a urinary marker consistent with improved oxidative DNA-damage repair during daytime sleep, supporting a biologically plausible link between circadian melatonin and genomic maintenance.35
For integrative oncology, this creates a larger framework: melatonin is not simply a sedative. It is a circadian signaling molecule that interacts with metabolic and cellular systems directly relevant to cancer.
RESEARCH OVERVIEW
1. Melatonin and Apoptosis
Apoptosis is programmed cell death. Cancer cells frequently acquire the ability to resist apoptosis, allowing damaged or genetically abnormal cells to survive.
Melatonin has been studied as an inducer or facilitator of apoptosis in multiple cancer models. Depending on the tumor type, experimental research has reported effects involving mitochondrial membrane signaling, caspases, BCL-2 family proteins, p53, endoplasmic-reticulum stress and reactive oxygen species.
This is particularly important because melatonin is often described only as an antioxidant. In some cancer cells, however, pharmacologic melatonin concentrations can behave very differently from normal physiologic nighttime levels and may contribute to pro-oxidant stress within the tumor cell, activating death pathways rather than protecting the malignant cell.
In cholangiocarcinoma cells, melatonin induced apoptosis through ROS-dependent DNA damage, providing a direct bile-duct-cancer example of this pro-oxidant mechanism.27
RESEARCH OVERVIEW
2. Melatonin, Mitochondria and Cancer Metabolism
Mitochondria are central to both normal metabolism and cancer biology.
Melatonin has been investigated for effects on mitochondrial respiration, oxidative phosphorylation, cellular redox balance and metabolic reprogramming. Cancer cells often shift toward increased glycolysis—the Warburg effect—even when oxygen is available.
A 2023 experimental study reported that melatonin altered pyruvate/lactate metabolism and opposed Warburg-type metabolic behavior in cancer cells.36
This is one of the most compelling areas for future melatonin research because tumor metabolism is directly connected to proliferation, survival, drug resistance and the tumor microenvironment.
RESEARCH OVERVIEW
3. Melatonin and Cell-Cycle Control
A malignant cell must repeatedly pass through the cell cycle to proliferate.
Melatonin has been shown in experimental systems to alter cyclins, proliferation markers and cell-cycle checkpoints. In androgen-sensitive prostate-cancer xenografts, melatonin reduced tumor growth and decreased expression of proliferating-cell nuclear antigen, cyclin A and PSA.23
This suggests that melatonin can act as a cytostatic signal in some tumors—slowing proliferation even when it does not immediately trigger cell death.
RESEARCH OVERVIEW
4. Anti-Angiogenic Effects: HIF-1α and VEGF
A growing tumor needs blood vessels.
Hypoxia-inducible factor 1-alpha (HIF-1α) helps tumors adapt to low oxygen and promotes expression of vascular endothelial growth factor (VEGF), one of the central drivers of angiogenesis.
Experimental research has shown that melatonin can destabilize hypoxia-induced HIF-1α and suppress tumor angiogenesis.18 Breast-cancer-related work has also shown reductions in VEGF/HIF-1α signaling and antiangiogenic effects in tumor and endothelial models.19
This gives melatonin a plausible role not only in affecting cancer-cell proliferation, but also in altering the tumor microenvironment required for continued growth.
RESEARCH OVERVIEW
5. Melatonin, EMT, Invasion and Metastasis
Metastasis requires cancer cells to detach, migrate, invade surrounding tissue, survive circulation and establish new tumors.
The epithelial-to-mesenchymal transition (EMT) is one process associated with increased migration and metastatic behavior.
In breast-cancer research, melatonin inhibited EMT-related signaling through Akt/GSK3β/β-catenin mechanisms.20 Other studies have reported suppression of metastatic behavior in HER2-positive breast-cancer cells and reductions in matrix-metalloproteinase-related signaling.
Melatonin has also inhibited migration in oral-cancer models and multiple other tumor systems.21
The importance of these findings is that melatonin research is not limited to whether a tumor cell divides. It extends into the pathways that may influence invasion and metastatic competence.
Cancer stem cells are tumor-cell populations with self-renewal and tumor-initiating properties. They are of particular interest because they may contribute to recurrence, metastasis and resistance to chemotherapy or radiation.
Melatonin has been studied directly against stem-like tumor populations.
BREAST CANCER
Breast Cancer Stem Cells
A 2016 study used three-dimensional mammosphere models containing CD44-positive/CD24-low stem-like breast-cancer cells. Melatonin reduced viability and invasiveness, increased E-cadherin, and reduced OCT4, N-cadherin and vimentin—changes consistent with suppression of stemness and EMT-related behavior.17
This is particularly interesting because OCT4 is associated with pluripotency and self-renewal, while the cadherin/vimentin changes reflect movement away from a mesenchymal, invasive phenotype.
RESEARCH OVERVIEW
Osteosarcoma Stem Cells
Melatonin has also been shown to inhibit osteosarcoma stem-cell sphere formation and alter EMT-related markers in experimental models.28
The cancer-stem-cell literature remains preclinical, but it adds another dimension to melatonin's potential role: the possibility of influencing tumor-initiating populations rather than only the bulk tumor mass.
BREAST CANCER
Breast Cancer: Estrogen Signaling and Aromatase
Melatonin has one of its strongest mechanistic research histories in breast cancer.
Human breast tumors and breast-cancer cell lines express melatonin receptors, particularly MT1.16 In estrogen-responsive breast-cancer systems, melatonin has been studied for anti-estrogenic effects including modulation of estrogen-receptor signaling and aromatase activity.
Experimental research has shown that melatonin can reduce aromatase activity and expression in breast-cancer-related models.37
This makes melatonin unusual among natural oncology compounds: it has a plausible connection to both circadian signaling and estrogen biology.
PROSTATE CANCER
Prostate Cancer: Androgen Signaling and Metabolic Regulation
Melatonin has also been studied in androgen-sensitive and castration-resistant prostate cancer.
In LNCaP prostate-cancer xenografts, melatonin inhibited growth in association with MT1 receptor expression and reduced PSA and proliferation markers.23
A 2021 study in advanced prostate-cancer models reported that melatonin altered lipid metabolism through epigenetic regulation of CES1, reduced intratumoral androgen synthesis and reversed enzalutamide resistance in experimental systems.24
A 2022 study likewise reported suppression of androgen-dependent prostate-cancer tumorigenesis.25
These are preclinical findings, but they connect melatonin to androgen signaling, lipid metabolism and endocrine-treatment resistance, all highly relevant areas in advanced prostate cancer.
Triple-negative breast cancer (TNBC) lacks estrogen receptor, progesterone receptor and HER2 expression. It is therefore especially important to identify non-estrogen-dependent pathways that may influence tumor behavior.
A 2021 study reported that melatonin inhibited TNBC progression through a lncRNA/FUNDC1-related pathway.29
A 2024 study found that melatonin increased olaparib sensitivity and reduced cancer-associated fibroblast infiltration through the LAMB3-CXCL2 axis in TNBC models.30
Even more recently, a 2026 study reported that melatonin suppressed TNBC progression through inhibition of FAK signaling and modulation of PD-L1 and the immune microenvironment.31
These findings remain preclinical, but together they make melatonin and triple-negative breast cancer an important emerging research area.
There is direct experimental research involving melatonin and cholangiocarcinoma.
A 2011 study found that cholangiocarcinoma cells can synthesize melatonin and suggested that an autocrine melatonin loop exerts antiproliferative effects; reduced endogenous melatonin synthesis was associated with cholangiocarcinoma growth.26
A separate study demonstrated that melatonin induced apoptosis in cholangiocarcinoma cells through ROS-dependent DNA damage.27
Animal research has also evaluated melatonin in cholangiocarcinoma-related liver injury and tumor biology.
This gives Sunridge a strong reason to link a future cholangiocarcinoma natural-compounds section directly to this melatonin research hub.
Lung cancer has some of the most important human data in the entire melatonin literature.
RESEARCH OVERVIEW
Early Advanced NSCLC Trials
Several older randomized studies from the same Italian research group used 20 mg of melatonin in the evening alongside chemotherapy or supportive care in advanced non-small cell lung cancer.
A 1997 randomized study compared cisplatin/etoposide alone with cisplatin/etoposide plus melatonin and reported improved survival and lower treatment toxicity with melatonin.5
A later randomized study followed 100 patients with metastatic NSCLC treated with cisplatin/etoposide with or without 20 mg nightly melatonin. Tumor regression was reported in 35% of the melatonin group versus 18% with chemotherapy alone, and three of 49 patients in the melatonin group were alive at five years while no chemotherapy-only patient survived beyond two years.4
These results are provocative, but they came from a small single research network and require independent confirmation.
CHEMOTHERAPY
A Modern Double-Blind Chemotherapy Trial
A 2014 randomized, double-blind placebo-controlled trial tested 10 mg or 20 mg melatonin during chemotherapy in advanced NSCLC. It did not show an improvement in survival or adverse-event rates, though there was a trend toward better health-related quality of life.2
RESEARCH OVERVIEW
The Large AMPLCaRe Trial
The most important modern lung-cancer study is the 2021 AMPLCaRe trial.
Seven hundred nine patients who had undergone complete resection of primary NSCLC were randomized to 20 mg melatonin nightly for one year or placebo. Across the full population, melatonin did not improve two-year or five-year disease-free survival.1
However, a prespecified stage-stratified analysis found a 25% relative hazard reduction in five-year disease-free survival among the smaller stage III/IV subgroup. The investigators considered that result promising but requiring confirmation.1
The most responsible interpretation is therefore:
Melatonin did not prevent recurrence across all surgically treated NSCLC patients, but advanced-stage subgroup findings remain interesting enough to justify further research.
Breast cancer may be the most biologically developed area of melatonin oncology research.
RESEARCH OVERVIEW
Melatonin and Tamoxifen
Small phase II studies from the 1990s evaluated melatonin with tamoxifen in metastatic breast cancer, including patients whose disease had progressed on tamoxifen alone. Those studies reported responses after melatonin was added to endocrine therapy.14
A separate randomized study evaluated tamoxifen alone versus tamoxifen plus melatonin in heavily pretreated estrogen-receptor-negative metastatic breast cancer and reported greater clinical activity in the combination arm.15
These studies are small and old, but they remain notable because melatonin's breast-cancer biology includes MT1 signaling, estrogen-receptor modulation and aromatase regulation.
CHEMOTHERAPY
Cognitive Function During Chemotherapy
A 2020 randomized double-blind placebo-controlled trial studied 20 mg melatonin around the first cycle of adjuvant breast-cancer chemotherapy. Melatonin improved several measures of executive function, episodic memory and verbal fluency, with associated improvements in sleep and depressive symptoms.10
This is supportive-care evidence, not evidence of tumor control, but it is clinically relevant.
RESEARCH OVERVIEW
Fatigue: Mixed Results
Melatonin has produced inconsistent results for breast-cancer-related fatigue.
One randomized trial using 18 mg/day during and after adjuvant treatment reported improvement in fatigue outcomes.32
By contrast, a phase III double-blind placebo-controlled trial in early-stage breast-cancer patients receiving radiotherapy found that melatonin did not significantly improve fatigue or other symptoms and was stopped early for futility.11
This is an excellent example of why melatonin should not be treated as universally beneficial for every cancer symptom.
Human colorectal-cancer data include a small randomized study of irinotecan.
Thirty patients with metastatic colorectal cancer progressing after 5-FU-containing therapy were randomized to weekly irinotecan alone or irinotecan plus 20 mg melatonin during the dark period. Disease control occurred in 12 of 14 patients receiving melatonin plus irinotecan versus seven of 16 receiving irinotecan alone.6
No complete responses occurred, and the study was small, but it provides direct randomized human evidence that justifies continued investigation.
Modern preclinical colorectal research continues to examine melatonin in relation to apoptosis, autophagy, drug resistance and oxaliplatin response.
Melatonin's ability to cross the blood-brain barrier makes brain-tumor research especially interesting.
A small randomized 1996 study compared radiotherapy alone with radiotherapy plus 20 mg/day melatonin in patients with glioblastoma. One-year survival was six of 14 in the melatonin arm versus one of 16 in the control arm, with lower radiation- or steroid-related toxicity reported in the melatonin group.7
That preliminary trial generated substantial interest, but it remains small and has not been confirmed in a large modern glioblastoma trial.
Melatonin also has extensive preclinical glioma research involving apoptosis, oxidative stress, melatonin receptors, metabolic signaling and interactions with temozolomide-related pathways.
The brain-metastasis literature provides a useful cautionary example.
An older randomized study in patients with brain metastases from solid tumors reported better survival and quality of life with supportive care plus melatonin compared with supportive care alone.8
However, the later Radiation Therapy Oncology Group phase II trial RTOG 0119 tested high-dose melatonin timed in the morning or evening with whole-brain radiotherapy and found no survival benefit compared with historical controls.9
So while small early studies were encouraging, a later cooperative-group trial did not reproduce a clear clinical benefit.
Melatonin has long-standing melanoma research, including clinical and emerging trial activity.
A randomized study published in 1996 evaluated adjuvant melatonin after treatment of lymph-node-relapsed malignant melanoma and reported longer disease-free survival in the melatonin group.33
The trial was small and predates modern immunotherapy.
Importantly, melatonin is now being tested again in a contemporary context. The AMUM phase III trial is evaluating long-term adjuvant melatonin in patients with high-risk uveal melanoma, with metastasis as the primary outcome.34
The existence of a modern phase III trial shows that melatonin remains a legitimate oncology research question rather than only a historical integrative therapy.
The prostate-cancer literature is primarily preclinical but mechanistically rich.
Melatonin inhibited androgen-sensitive LNCaP xenograft growth and reduced PSA and proliferation markers in association with MT1 receptor expression.23
More recent work links melatonin to lipid metabolism, intratumoral androgen synthesis and enzalutamide resistance through CES1-related epigenetic regulation.24
Other studies have reported effects on androgen-receptor signaling and prostate-tumor apoptosis.25
This makes melatonin particularly interesting for future research in androgen-dependent disease and castration-resistant prostate cancer.
RESEARCH OVERVIEW
Ovarian and Gynecologic Cancer
Laboratory studies have reported melatonin-induced apoptosis and modulation of survival signaling in ovarian and other gynecologic cancer models. Melatonin's reproductive-hormone biology and mitochondrial activity make this an active area of experimental study.
RESEARCH OVERVIEW
Leukemia
Melatonin has demonstrated pro-apoptotic and redox effects in leukemia models. Research has examined oxidative stress, mitochondrial signaling and the possibility of differential effects on malignant versus normal hematopoietic cells.
RESEARCH OVERVIEW
Osteosarcoma
Melatonin has inhibited osteosarcoma stem-cell sphere formation and altered EMT-related pathways.28
Melatonin cancer research includes circadian biology, apoptosis, EMT, cancer stem cells, angiogenesis and hormone-related signaling.
RESEARCH OVERVIEW
Oral and Head-and-Neck Cancer
Melatonin has reduced migration in oral-cancer models through pathways involving matrix metalloproteinases and metastatic signaling.21
RESEARCH OVERVIEW
Liver Cancer
Hepatocellular-carcinoma research has explored melatonin in relation to apoptosis, oxidative stress, autophagy, angiogenesis and metabolic signaling.
One of the central questions in integrative oncology is whether melatonin can be combined with chemotherapy.
The answer is not simply yes or no.
Older randomized trials reported improved response or lower toxicity when melatonin was combined with cisplatin/etoposide in NSCLC, irinotecan in colorectal cancer and other chemotherapy regimens.46
A 1999 randomized study of metastatic solid-tumor patients with poor performance status also reported higher response and lower rates of several toxicities when 20 mg nightly melatonin was added to chemotherapy.3
But not all trials have been positive.
A double-blind study using 40 mg/day melatonin in lung-cancer patients receiving carboplatin/etoposide found no myeloprotective effect.38
And the modern 2014 NSCLC chemotherapy trial found no survival or toxicity benefit with 10 or 20 mg melatonin.2
The practical lesson is that melatonin should be evaluated in the context of the specific cancer, drugs, dose, timing and treatment objective.
Melatonin is especially interesting in radiation research because it may produce different effects in normal cells and cancer cells.
Experimental work has investigated melatonin as a radioprotector of normal tissues and as a radiosensitizer in some tumors.
Human evidence is mixed. The small glioblastoma trial reported better one-year survival with radiation plus melatonin.7 The later RTOG brain-metastasis trial did not demonstrate a survival advantage.9
Breast-cancer symptom trials during radiotherapy have also produced conflicting results, with some recent studies reporting symptom improvement while a phase III fatigue trial did not.11
For this reason, radiation-related use should be individualized rather than based on the assumption that melatonin always protects or always sensitizes.
Melatonin interacts with immune signaling at multiple levels.
Older clinical programs combined melatonin with interleukin-2, based on proposed neuroendocrine-immune interactions. Modern preclinical research is beginning to examine more specific immune-oncology pathways.
A 2026 TNBC study reported that melatonin inhibited FAK signaling and altered PD-L1-associated immune biology in experimental systems.31
This area is potentially important for checkpoint-inhibitor-era oncology, but it remains preclinical. Patients receiving immunotherapy require particular care because any compound capable of modifying immune signaling should be considered within the complete immune-treatment context.
This is one of the most important questions to address honestly.
Melatonin is a powerful antioxidant and can protect normal cells from oxidative injury. That raises a reasonable concern when chemotherapy or radiation partly relies on oxidative damage.
But melatonin's cancer biology is more complex than the word “antioxidant” suggests.
In many cancer models, melatonin can increase oxidative stress, destabilize tumor survival pathways, promote apoptosis or inhibit metabolism while simultaneously protecting normal tissues from excessive oxidative injury.
That selective behavior is biologically attractive, but it is not guaranteed with every cancer or treatment.
The correct conclusion is not that melatonin automatically interferes with treatment—and not that it automatically enhances treatment.
The combination needs to be evaluated drug by drug, cancer by cancer and schedule by schedule.
Cancer studies have used doses very different from the small doses often used for sleep.
Examples include:
- 3 mg nightly in some breast-cancer survivor sleep/biomarker studies.
- 6 mg in perioperative or supportive breast-cancer studies.
- 10 mg and 20 mg nightly in a modern chemotherapy trial in advanced NSCLC.2
- 18 mg/day in a randomized breast-cancer fatigue study.32
- 20 mg nightly in many of the historical oncology trials and in the large AMPLCaRe lung-cancer trial.1
- 40 mg/day in a double-blind lung-cancer myeloprotection study.38
- Higher experimental doses have been investigated in radiation and other research settings, but high-dose use remains investigational.
These are research doses, not a universal treatment protocol.
The dose used for insomnia should not automatically be assumed to be the dose being studied for cancer biology, and the dose used in one cancer cannot automatically be transferred to another.
Melatonin is a chronobiotic hormone. Timing is therefore biologically relevant.
Many oncology trials administered melatonin in the evening or during the dark period, often at approximately the same time each night.46
This makes sense physiologically because endogenous melatonin is a nighttime signal.
However, some experimental oncology strategies explore timing outside the conventional sleep window to exploit pharmacologic rather than circadian effects. That remains an investigational area.
At Sunridge Medical, timing should be treated as part of the therapeutic plan rather than as an afterthought.
Even when melatonin's direct antitumor effect is uncertain, it may still have value in supportive oncology.
CHEMOTHERAPY
Cognition During Chemotherapy
The 2020 randomized breast-cancer chemotherapy trial reported improvements in executive function, episodic memory and verbal fluency with melatonin.10
RESEARCH OVERVIEW
Sleep and Mood
Several breast-cancer studies have examined melatonin for sleep disturbance, depressive symptoms and treatment-related quality of life. Outcomes are generally more favorable for sleep than for direct anticancer endpoints.
RESEARCH OVERVIEW
Fatigue
Fatigue results are inconsistent.
A 2015 double-blind crossover trial in advanced cancer found that 20 mg melatonin did not improve fatigue or other symptoms.39
The large AMPLCaRe study also did not show meaningful improvements in fatigue, sleep, depression, anxiety or pain across the full NSCLC population.1
So melatonin should not be promised as a universal fatigue treatment.
A large portion of the positive human cancer literature came from one Italian research network in the 1990s and early 2000s.
Those trials are important because they were randomized, used clinically meaningful endpoints and repeatedly reported favorable findings.
But they also have limitations:
- Many were small.
- Several were single-center.
- Treatment regimens reflect an older era of oncology.
- Some results have not been replicated independently.
- Modern standards for trial registration, allocation reporting and endpoint analysis were not always used.
The newer evidence is more mixed.
The 709-patient AMPLCaRe lung-cancer trial found no overall disease-free-survival benefit.1 The 2014 NSCLC chemotherapy trial did not reproduce older survival findings.2 Modern supportive-care trials have also produced both positive and negative results.
This does not make the older work irrelevant.
It means melatonin deserves more high-quality modern trials—not less attention.
Melatonin has several characteristics that make it different from many supplements marketed to cancer patients.
It is:
- An endogenous human hormone.
- A central circadian signal.
- Able to cross biological membranes and the blood-brain barrier.
- Connected to mitochondrial metabolism.
- Active through MT1/MT2 receptors and intracellular mechanisms.
- Studied in apoptosis, angiogenesis, EMT, cancer stem cells and metabolic reprogramming.
- Supported by human randomized oncology trials, even though results are inconsistent.
- Generally inexpensive and well tolerated in the studied oral doses.
- Currently being investigated in modern phase III oncology research, including high-risk uveal melanoma.34
That combination makes melatonin one of the more scientifically interesting natural agents in integrative oncology.
At Sunridge Medical, melatonin should be considered within the context of the entire cancer case.
Important factors may include:
- Cancer type and stage.
- Molecular and receptor characteristics.
- Current chemotherapy.
- Radiation schedule.
- Immunotherapy.
- Endocrine treatment.
- Targeted therapy.
- Neurologic status.
- Sleep-wake cycle and circadian disruption.
- Liver and kidney function.
- Sedating medications.
- Anticoagulants and other medications.
- Previous treatment response.
- Treatment-related fatigue, sleep disturbance or cognitive symptoms.
- Whether the objective is direct tumor biology, treatment support, circadian restoration or a combination of goals.
This is very different from simply adding a sleep supplement.
Sunridge Medical in Scottsdale, Arizona focuses on integrative and naturopathic approaches to complex cancer cases.
Depending upon the patient, an integrative oncology program may include physician-directed natural compounds, IV therapies, metabolic medicine, botanical medicine, hyperthermia, mistletoe, nutritional medicine and other strategies selected around the patient's diagnosis and current oncology treatment.
Melatonin can fit naturally into this approach because it intersects with multiple areas that matter in cancer biology:
circadian signaling, mitochondrial metabolism, apoptosis, angiogenesis, hormone signaling, stemness, treatment response and supportive care.
The strongest use of melatonin is not to treat it as a miracle therapy.
It is to understand where its biology is relevant, where human evidence exists, where the evidence is still preclinical, and how to use that information intelligently within a broader treatment plan.
RESEARCH OVERVIEW
Is melatonin only useful for sleep?
No. Melatonin is a circadian hormone with receptor-mediated and intracellular effects on metabolism, oxidative signaling, mitochondrial function, hormone pathways and cell growth. Sleep is only one part of its biology.
RESEARCH OVERVIEW
Has melatonin been studied in cancer patients?
Yes. Randomized human trials have been conducted in non-small cell lung cancer, breast cancer, colorectal cancer, glioblastoma, brain metastases and advanced solid tumors.
RESEARCH OVERVIEW
What dose of melatonin is used for cancer?
There is no universally established oncology dose. Human cancer studies have used doses ranging from a few milligrams to 40 mg/day, with 20 mg nightly being common in several historical oncology trials. Study doses should not be interpreted as a universal treatment recommendation.
RESEARCH OVERVIEW
Does melatonin kill cancer cells?
In laboratory models, melatonin can induce apoptosis, inhibit proliferation, alter metabolism, reduce angiogenesis and suppress invasion in multiple cancer types. Whether those effects translate into meaningful clinical benefit depends on the cancer, dose, formulation and treatment context.
RESEARCH OVERVIEW
Does melatonin affect cancer stem cells?
Yes, in preclinical research. Breast-cancer mammosphere studies have shown effects on stemness and EMT markers, and osteosarcoma research has shown reduced stem-cell sphere formation.
RESEARCH OVERVIEW
Is melatonin being studied in triple-negative breast cancer?
Yes. Recent TNBC research includes FUNDC1-related signaling, olaparib sensitization, fibroblast infiltration, FAK signaling and PD-L1-associated immune biology.
RESEARCH OVERVIEW
Has melatonin been studied in cholangiocarcinoma?
Yes. Cholangiocarcinoma research has reported antiproliferative autocrine melatonin signaling and ROS-dependent apoptosis after pharmacologic melatonin exposure.
RESEARCH OVERVIEW
Has melatonin been studied in lung cancer?
Yes. Lung cancer has both older positive randomized studies and more recent mixed or negative trials. It is one of the most clinically studied cancer types for melatonin.
RESEARCH OVERVIEW
Can melatonin be used during chemotherapy?
Possibly, but this should be physician-directed. Some studies suggest benefit when melatonin is combined with selected chemotherapy regimens, while other trials show no benefit. Drug, dose and timing matter.
RESEARCH OVERVIEW
Can melatonin be used during radiation?
Melatonin has been studied as both a normal-tissue radioprotector and a tumor radiosensitizer. Human results are mixed, so radiation-related use should be individualized.
RESEARCH OVERVIEW
Is high-dose melatonin safe?
Melatonin has generally been well tolerated in cancer trials using 10–40 mg/day, but higher-dose pharmacologic use is different from ordinary sleep supplementation and should be medically supervised.
RESEARCH OVERVIEW
Does Sunridge Medical use melatonin in cancer care?
Melatonin may be considered as one component of an individualized physician-directed integrative oncology program when clinically appropriate.
Melatonin may be one of the most underestimated molecules in integrative oncology.
It is produced naturally by the human body.
It coordinates circadian biology.
It interacts with mitochondria.
It can influence estrogen and androgen pathways.
It has been studied in cancer stem cells.
It can alter apoptosis, angiogenesis, EMT, metabolism and immune signaling.
And unlike many natural compounds, it has been tested in randomized human cancer trials.
The evidence is not uniform, and melatonin should not be presented as a proven stand-alone cancer cure.
But the breadth of the science justifies taking melatonin seriously as a physician-directed integrative oncology tool.
For patients seeking a more individualized approach to cancer care, Sunridge Medical can review your diagnosis, current treatment, laboratory findings, medications and goals and determine whether melatonin or other integrative therapies may fit within your treatment strategy.
Call Sunridge Medical at 1-800-923-7878 to speak with our Patient Care Team.
1. Seely D, et al. Adjuvant melatonin for the prevention of recurrence and mortality following lung cancer resection (AMPLCaRe): a randomized placebo-controlled clinical trial. EClinicalMedicine. 2021. PMID: 33681747. <a href="https://pubmed.ncbi.nlm.nih.gov/33681747/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/33681747/</a>
2. Sookprasert A, et al. Melatonin in patients with cancer receiving chemotherapy: a randomized, double-blind, placebo-controlled trial. Anticancer Research. 2014. PMID: 25503168. <a href="https://pubmed.ncbi.nlm.nih.gov/25503168/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/25503168/</a>
3. Lissoni P, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer. 1999. PMID: 10674014. <a href="https://pubmed.ncbi.nlm.nih.gov/10674014/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/10674014/</a>
4. Lissoni P, et al. Five years survival in metastatic non-small cell lung cancer patients treated with chemotherapy alone or chemotherapy and melatonin: a randomized trial. J Pineal Res. 2003. PMID: 12823608. <a href="https://pubmed.ncbi.nlm.nih.gov/12823608/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/12823608/</a>
5. Lissoni P, et al. A randomized study of chemotherapy with cisplatin plus etoposide versus chemoendocrine therapy with cisplatin, etoposide and melatonin in advanced NSCLC. J Pineal Res. 1997. PMID: 9379341. <a href="https://pubmed.ncbi.nlm.nih.gov/9379341/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/9379341/</a>
6. Cerea G, et al. Biomodulation of cancer chemotherapy for metastatic colorectal cancer: irinotecan alone versus irinotecan plus melatonin. Anticancer Res. 2003. PMID: 12820485. <a href="https://pubmed.ncbi.nlm.nih.gov/12820485/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/12820485/</a>
7. Lissoni P, et al. Increased survival time in brain glioblastomas by radiotherapy plus melatonin compared to radiotherapy alone. Oncology. 1996. PMID: 8570130. <a href="https://pubmed.ncbi.nlm.nih.gov/8570130/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/8570130/</a>
8. Lissoni P, et al. A randomized study with melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer. 1994. PMID: 8299092. <a href="https://pubmed.ncbi.nlm.nih.gov/8299092/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/8299092/</a>
9. Berk L, et al. Randomized phase II trial of high-dose melatonin and radiation therapy for patients with brain metastases (RTOG 0119). Int J Radiat Oncol Biol Phys. 2007. PMID: 17418968. <a href="https://pubmed.ncbi.nlm.nih.gov/17418968/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/17418968/</a>
10. Palmer ACS, et al. Clinical impact of melatonin on breast cancer patients undergoing chemotherapy; effects on cognition, sleep and depressive symptoms. PLoS One. 2020. PMID: 32302347. <a href="https://pubmed.ncbi.nlm.nih.gov/32302347/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/32302347/</a>
11. Mukhopadhyay ND, et al. Melatonin supplementation for cancer-related fatigue in patients with early-stage breast cancer receiving radiotherapy. Oncologist. 2024. PMID: 37699115. <a href="https://pubmed.ncbi.nlm.nih.gov/37699115/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/37699115/</a>
12. Schernhammer ES, et al. A randomized controlled trial of oral melatonin supplementation and breast cancer biomarkers. Cancer Causes Control. 2012. PMID: 22370698. <a href="https://pubmed.ncbi.nlm.nih.gov/22370698/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/22370698/</a>
13. Pashaki AS, et al. A randomized controlled trial on melatonin and fatigue during adjuvant treatment of breast cancer. 2021. PMID: 33543655. <a href="https://pubmed.ncbi.nlm.nih.gov/33543655/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/33543655/</a>
14. Lissoni P, et al. Modulation of cancer endocrine therapy by melatonin: tamoxifen plus melatonin in metastatic breast cancer progressing under tamoxifen alone. Br J Cancer. 1995. PMID: 7710954. <a href="https://pubmed.ncbi.nlm.nih.gov/7710954/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/7710954/</a>
15. Lissoni P, et al. Tamoxifen alone versus tamoxifen plus melatonin in ER-negative heavily pretreated metastatic breast cancer. Oncology. 1995. PMID: 21597833. <a href="https://pubmed.ncbi.nlm.nih.gov/21597833/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/21597833/</a>
16. Lai L, et al. Alteration of the MT1 melatonin receptor gene and its expression in primary human breast tumors and breast cancer cell lines. Breast Cancer Res Treat. 2009. PMID: 18979234. <a href="https://pubmed.ncbi.nlm.nih.gov/18979234/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/18979234/</a>
17. Gonçalves NDN, et al. Effect of melatonin in EMT markers and invasive properties of breast cancer stem cells. PLoS One. 2016. PMID: 26934679. <a href="https://pubmed.ncbi.nlm.nih.gov/26934679/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/26934679/</a>
18. Park SY, et al. Melatonin suppresses tumor angiogenesis by inhibiting HIF-1α stabilization under hypoxia. 2010. PMID: 20449875. <a href="https://pubmed.ncbi.nlm.nih.gov/20449875/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/20449875/</a>
19. Dai M, et al. Melatonin modulates VEGF and HIF-1α expression in cancer-related hypoxic signaling. 2008. PMID: 18289162. <a href="https://pubmed.ncbi.nlm.nih.gov/18289162/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/18289162/</a>
20. Mao L, et al. Circadian gating of epithelial-to-mesenchymal transition in breast cancer cells via melatonin-related signaling. 2012. PMID: 23002080. <a href="https://pubmed.ncbi.nlm.nih.gov/23002080/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/23002080/</a>
21. Yeh CM, et al. Melatonin inhibits TPA-induced oral cancer cell migration by reducing metastatic signaling. 2016. PMID: 26980735. <a href="https://pubmed.ncbi.nlm.nih.gov/26980735/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/26980735/</a>
22. Mao L, et al. Melatonin represses metastasis in HER2-positive human breast cancer cells. 2016. PMID: 27535706. <a href="https://pubmed.ncbi.nlm.nih.gov/27535706/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/27535706/</a>
23. Xi SC, et al. Inhibition of androgen-sensitive LNCaP prostate cancer growth in vivo by melatonin. Prostate. 2001. PMID: 11170132. <a href="https://pubmed.ncbi.nlm.nih.gov/11170132/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/11170132/</a>
24. Zhou L, et al. Melatonin inhibits lipid accumulation to repress prostate cancer progression by epigenetic modification of CES1. Clin Transl Med. 2021. PMID: 34185414. <a href="https://pubmed.ncbi.nlm.nih.gov/34185414/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/34185414/</a>
25. Hao L, et al. Melatonin decreases androgen-sensitive prostate cancer tumorigenesis. 2022. PMID: 35242644. <a href="https://pubmed.ncbi.nlm.nih.gov/35242644/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/35242644/</a>
26. Han Y, et al. Melatonin exerts an autocrine antiproliferative effect in cholangiocarcinoma; its synthesis is reduced favoring tumor growth. 2011. PMID: 21778461. <a href="https://pubmed.ncbi.nlm.nih.gov/21778461/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/21778461/</a>
27. Laothong U, et al. Melatonin induces apoptosis in cholangiocarcinoma cells through ROS-dependent DNA damage. 2015. PMID: 25606968. <a href="https://pubmed.ncbi.nlm.nih.gov/25606968/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/25606968/</a>
28. Qu H, et al. Melatonin inhibits osteosarcoma stem cells by suppressing stemness and EMT-related pathways. 2018. PMID: 29689273. <a href="https://pubmed.ncbi.nlm.nih.gov/29689273/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/29689273/</a>
29. Yang A, et al. Melatonin inhibits triple-negative breast cancer progression through the lnc049808-FUNDC1 pathway. 2021. PMID: 34272359. <a href="https://pubmed.ncbi.nlm.nih.gov/34272359/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/34272359/</a>
30. Lai YW, et al. Melatonin increases olaparib sensitivity and suppresses cancer-associated fibroblast infiltration in TNBC. 2024. PMID: 39306019. <a href="https://pubmed.ncbi.nlm.nih.gov/39306019/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/39306019/</a>
31. Wu CC, et al. Melatonin inhibits FAK signaling to suppress PD-L1-associated progression in triple-negative breast cancer. 2026. PMID: 41799764. <a href="https://pubmed.ncbi.nlm.nih.gov/41799764/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/41799764/</a>
32. Pashaki AS, et al. Long-term melatonin and fatigue in breast cancer patients receiving adjuvant therapy. 2023. PMID: 37139718. <a href="https://pubmed.ncbi.nlm.nih.gov/37139718/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/37139718/</a>
33. Lissoni P, et al. Adjuvant therapy with melatonin in patients with lymph-node relapse due to malignant melanoma. J Pineal Res. 1996. PMID: 8989723. <a href="https://pubmed.ncbi.nlm.nih.gov/8989723/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/8989723/</a>
34. Kal Omar R, et al. Adjuvant melatonin for uveal melanoma (AMUM): protocol for a randomized open-label phase III study. Trials. 2023. PMID: 36966349. <a href="https://pubmed.ncbi.nlm.nih.gov/36966349/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/36966349/</a>
35. Zanif U, et al. Melatonin supplementation and oxidative DNA damage repair capacity among night shift workers: a randomized placebo-controlled trial. Occup Environ Med. 2025. PMID: 39993913. <a href="https://pubmed.ncbi.nlm.nih.gov/39993913/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/39993913/</a>
36. Cruz EMS, et al. Melatonin modulates the Warburg effect and alters pyruvate/lactate metabolism in cancer cells. 2023. PMID: 36863486. <a href="https://pubmed.ncbi.nlm.nih.gov/36863486/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/36863486/</a>
37. Alvarez-García V, et al. Melatonin modulates aromatase activity and expression in breast-cancer-related models. 2013. PMID: 23450505. <a href="https://pubmed.ncbi.nlm.nih.gov/23450505/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/23450505/</a>
38. Ghielmini M, et al. Double-blind randomized study on the myeloprotective effect of melatonin with carboplatin and etoposide in advanced lung cancer. 1999. PMID: 10362116. <a href="https://pubmed.ncbi.nlm.nih.gov/10362116/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/10362116/</a>
39. Rasmussen CL, et al. Effects of melatonin on physical fatigue and other symptoms in patients with advanced cancer receiving palliative care. Cancer. 2015. PMID: 26178160. <a href="https://pubmed.ncbi.nlm.nih.gov/26178160/" target="_blank" rel="noopener">https://pubmed.ncbi.nlm.nih.gov/26178160/</a>
BECOME A PATIENT
Explore Physician-Directed Integrative Cancer Care with Melatonin
Melatonin is one of the most extensively studied natural compounds in integrative oncology, with research spanning circadian biology, lung cancer, breast cancer, colorectal cancer, glioblastoma, triple-negative breast cancer, cholangiocarcinoma and supportive oncology.
Speak with our Patient Care Team about your diagnosis, current treatment and whether melatonin may fit within a broader physician-directed treatment strategy.
RESEARCH
References
Research organized by cancer type
Browse 41 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked cancer type to move directly to its corresponding Sunridge page.
Melatonin Inhibits Chemical Carcinogen-mediated Malignant Transformation of Urothelial Cells: In Vitro Evidence.
In the in vitro system with carcinogen challenge, melatonin significantly prevented the neoplastic transformation of SV-HUC-1 cells.
Melatonin Inhibits EMT in Bladder Cancer by Targeting Autophagy.
The mechanisms of action of melatonin against tumor progression involve cellular apoptosis, antimetastatic activity, antioxidant and mutagenic effects, antiangiogenic activity, and the restoration of cancer immune surveillance.
Melatonin attenuates bone cancer pain via the SIRT1/HMGB1 pathway.
Moreover, mice in the melatonin group exhibited an increase in SIRT1 and nucleus-HMGB1, whilst there was a decrease in HMGB1, cytoplasm-HMGB1, rage, acetyl-HMGB1 and inflammatory cytokines compared with those in BCP mice.
Melatonin Increases the Sensitivity of Osteosarcoma Cells to Chemotherapy Drug Cisplatin.
In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.
A natural compound melatonin enhances the effects of Nimotuzumab via inhibiting EGFR in glioblastoma.
This proposition was validated in our in vitro and in vivo studies where melatonin synergistically augmented cytotoxicity and apoptosis in Nimotuzumab-treated glioma cells.
Glioblastoma progression is hindered by melatonin-primed mesenchymal stromal cells through dynamic intracellular and extracellular reorganizations.
This study investigates how MSCs influence tumor behavior and explores the synergistic anticancer effects in combination with melatonin (Mel).
Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/ERK/STAT3 Signalling.
Restoration of these factors suppressed glioma cell proliferation, migration and invasion while promoting apoptosis.
Inhibition of autophagy triggers melatonin-induced apoptosis in glioblastoma cells.
Remarkably, co-treatment with 3-MA and melatonin significantly enhanced the apoptotic cell population in the glioblastoma cells, along with a prominent decrease in the expression of bcl-2 and increase in the Bax expression levels, which collectively indicated that the disruption of autophagy triggers the melatonin-induced apoptosis in glioblastoma cells.
Melatonin Synergises the Chemotherapeutic Effect of Temozolomide in Glioblastoma by Suppressing NF-κB/COX-2 Signalling Pathways.
Melatonin (Mel), a natural indoleamine synthesised by the pineal gland, has demonstrated synergistic anti-tumour effects when combined with various chemotherapy agents in multiple studies.
Effects of Melatonin and Doxorubicin on Primary Tumor And Metastasis in Breast Cancer Model.
Tumor growth and metastasis were markedly suppressed in melatonin alone and in combination with doxorubicin.
Melatonin inhibits breast cancer cell invasion through modulating DJ-1/KLF17/ID-1 signaling pathway.
Melatonin and taxol clearly decreased cell migration and invasion at low doses, especially those matching the normal physiological concentration at night.
The evaluation of melatonin and EGF interaction on breast cancer metastasis.
The results of this study show that melatonin in the presence of EGF does not show the anti-cancer properties previously described for this substance.
Retraction Note: Melatonin enhances TNF-α-mediated cervical cancer HeLa cells death via suppressing CaMKII/Parkin/mitophagy axis.
The study reports retraction Note: Melatonin enhances TNF-α-mediated cervical cancer HeLa cells death via suppressing CaMKII/Parkin/mitophagy axis.
Targeting mitochondrial ribosomal protein expression by andrographolide and melatonin for colon cancer treatment.
Little is known about the role of mitochondria in the survival and metastatic ability of CSCs.
Melatonin Inhibits Gastric Cancer Cell Proliferation by Suppressing Exosome miR-27b-3p Expression.
In addition to its established role in regulating circadian rhythms and reducing inflammation, melatonin has been demonstrated to possess anti-cancer properties.
A novel melatonin-regulated lncRNA suppresses TPA-induced oral cancer cell motility through replenishing PRUNE2 expression.
Downregulation of MROS-1 by melatonin suppressed TPA-induced oral cancer migration through replenishing the protein expression of prune homolog 2 (PRUNE2), which functioned as a tumor suppressor in oral cancer.
Clinical significance of serum melatonin in predicting the severity of oral squamous cell carcinoma.
Melatonin, the primary hormone produced by the pineal gland, is intensely assessed for its anticancer properties.
Effects of melatonin receptor expression on prognosis and survival in oral squamous cell carcinoma patients.
A Cox proportional-hazard model showed that melatonin receptor 1A may serve as a significant predictor of the survival rate of patients with oral squamous cell carcinoma [hazard ratio = 1.423, 95% confidence interval (CI) = 1.019-1.988, p = 0.038].
Melatonin and erastin emerge synergistic anti-tumor effects on oral squamous cell carcinoma by inducing apoptosis, ferroptosis, and inhibiting autophagy through promoting ROS.
Combined treatment of melatonin and erastin markedly reduced the tumor size in vivo, demonstrated no obvious systemic side effects, and significantly enhanced the apoptosis and ferroptosis levels in the tumor tissues, in parallel with decreased autophagy levels.
Melatonin drives apoptosis in head and neck cancer by increasing mitochondrial ROS generated via reverse electron transport.
We found that genetic manipulation of cancer cells with alternative oxidase, which transfers electrons from QH2 to oxygen, inhibited melatonin-induced ROS generation, and apoptosis.
Melatonin exerts anti-oral cancer effect via suppressing LSD1 in patient-derived tumor xenograft models.
Our results indicated that melatonin, at pharmacological concentrations, significantly suppresses cell proliferation in a dose- and time-dependent manner.
Melatonin Exerts Anticancer Effects in Human Tongue Squamous Cell Carcinoma Cells by Promoting Autophagy.
We found that melatonin treatment significantly reduced the viability and colony formation ability of SCC-25 cells, impairing cell migration and invasion.
Melatonin inhibits the stemness of head and neck squamous cell carcinoma by modulating HA synthesis via the FOSL1/HAS3 axis.
In this study, we found that melatonin suppressed CSC-related markers, such as CD44, of HNSCC cells and decreased the tumor-initiating frequency of CSCs in vivo.
Melatonin modulates metabolic remodeling in HNSCC by suppressing MTHFD1L-formate axis.
Furthermore, we found that melatonin inhibited the expression of MTHFD1L in HNSCC cells through the downregulation of cyclic AMP-responsive element-binding protein 1 (CREB1) phosphorylation.
Melatonin represses oral squamous cell carcinoma metastasis by inhibiting tumor-associated neutrophils.
Overall, The beneficial roles of melatonin in retarding OSCC metastasis were implicated with inhibition of TANs.
Melatonin reverses nasopharyngeal carcinoma cisplatin chemoresistance by inhibiting the Wnt/β-catenin signaling pathway.
Melatonin not only reversed DDP chemoresistance, but also enhanced DDP antitumor activity by suppressing the nuclear translocation of β-catenin, and reducing expression of Wnt/β-catenin response genes in NPC cells.
Melatonin Targets Metabolism in Head and Neck Cancer Cells by Regulating Mitochondrial Structure and Function.
We found that melatonin increases oxidative phosphorylation (OXPHOS) and inhibits glycolysis in HNSCC, resulting in increased ROS production, apoptosis, and mitophagy, and decreased cell proliferation.
Melatonin inhibits MLL-rearranged leukemia via RBFOX3/hTERT and NF-κB/COX-2 signaling pathways.
In this study, melatonin inhibited cell proliferation and induced apoptosis by activating the caspase-dependent apoptotic pathway in MLL-r leukemia cells.
Melatonin Downregulates PD-L1 Expression and Modulates Tumor Immunity in KRAS-Mutant Non-Small Cell Lung Cancer.
In the present study, melatonin treatment significantly reduced cell viability accompanied by inducing cell apoptosis in KRAS-mutant NSCLC cell lines including A549, H460, and LLC1 cells.
Amelioration of Dalton's lymphoma-induced angiogenesis by melatonin.
Dalton's lymphoma ascites induced significant increase in endothelial cell proliferation, migration, and sprouting of the tertiary branching in chorioallantoic membrane and mesentery of Dalton's lymphoma-bearing mice, whereas melatonin treatment led to their inhibition in a dose-dependent manner.
Melatonin and Metformin Failed to Modify the Effect of Dacarbazine in Melanoma.
Current data support the possibility of antitumor activity of melatonin and metformin.
Melatonin Receptor Expression in Primary Uveal Melanoma.
Melatonin, noted for its anti-cancer properties in various malignancies, including cutaneous melanoma, shows promise in Uveal melanoma (UM) treatment.
Melatonin changes energy metabolism and reduces oncogenic signaling in ovarian cancer cells.
Because melatonin (Mel) has antitumor actions, we investigated its impact on energy metabolism and kinase signaling in OC cells (SKOV-3 and CAISMOV-24).
The proteomic landscape of ovarian cancer cells in response to melatonin.
We conclude that melatonin significantly alters the proteome of SKOV-3 cells by changing proteins involved with the immune response and mitochondrial metabolism.
Melatonin decreases androgen-sensitive prostate cancer growth by suppressing SENP1 expression.
Herein, we report that melatonin has the ability to decrease the growth and metastasis of androgen-dependent prostate cancer.
Melatonin impedes prostate cancer metastasis by suppressing MMP-13 expression.
Importantly, tumor growth rate and metastasis to distant organs were suppressed by melatonin in an orthotopic prostate cancer model.
Targeting Melatonin to Mitochondria Mitigates Castration-Resistant Prostate Cancer by Inducing Pyroptosis.
The modification of melatonin (Mel) to a triphenylphosphonium (TPP) cation-targeted mitochondria-melatonin (Mito-Mel) significantly increases its potency by over 1000-fold.
Liquid-Liquid Phase Separation of AR Orchestrated by Melatonin Sensitizes Prostate Cancer to Ferroptosis Via MCM5/NRF2 Axis Collapse.
We found that MEL effectively inhibited PCa proliferation, migration, and invasion in vitro while suppressing tumor growth safely in mice models.
Melatonin Increases the Sensitivity of Osteosarcoma Cells to Chemotherapy Drug Cisplatin.
In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.
Exploring the therapeutic effect of melatonin targeting common biomarkers in testicular germ cell tumor, prostate adenocarcinoma, and male infertility: an integrated biology approach.
The gene ontologies and pathway enrichment analysis were done for these significant genes in response to identifying and accessing the involvement of these genes in other processes.
Melatonin suppresses tumor proliferation and metastasis by targeting GATA2 in endometrial cancer.
In addition, in vivo and in vitro experiments showed that MT inhibited the proliferation and metastasis of EC cells by upregulating GATA2 expression.
No studies match those filters. Clear a filter or try a broader term.
