RESEARCH & NATURAL MEDICINE
Curcumin products vary widely in dose, absorption and route. A physician can review whether the goal is symptom support, nutrition, an investigational IV approach or another part of integrative cancer care—and coordinate it with current treatment.
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Few natural compounds have generated as much interest in cancer research as curcumin, the bright yellow polyphenol derived from turmeric. Curcumin has been investigated across apoptosis, cancer stem cells, NF-κB, STAT3, PI3K/AKT/mTOR, inflammatory signaling, angiogenesis, invasion, metastasis, chemotherapy sensitivity, radiation sensitivity and cancer metabolism.
At Sunridge Medical in Scottsdale, Arizona, curcumin may be considered as part of a physician-directed integrative oncology program based upon the individual patient’s diagnosis, current treatment, medications, laboratory findings and overall oncology strategy.
This page reviews the relationship between curcumin and cancer, including human clinical studies, chemotherapy combinations, apoptosis pathways, cancer stem-cell research and radiation-sensitization studies.
Curcumin is a turmeric-derived polyphenol studied across multiple cancer-related pathways.
MULTI-TARGETED CANCER RESEARCH
Cancer is driven by interconnected biological systems. A tumor may simultaneously alter cell growth, inflammation, apoptosis, metabolism, angiogenesis, invasion and resistance to treatment.
Curcumin is unusual because researchers have reported effects across many of these systems rather than on one molecular target alone.
The National Cancer Institute notes that curcumin research has examined pathways involving cell-cycle proteins, apoptosis, proliferation, PI3K/AKT survival signaling, MMP-9, VEGF, CXCR4 and inflammatory mediators including NF-κB, TNF, IL-1, IL-8 and COX-2.1
PROGRAMMED CELL DEATH
One of the most extensively studied effects of curcumin is its ability to induce apoptosis, the organized cellular program that allows abnormal cells to initiate their own death sequence.
Cancer cells frequently become resistant to apoptotic signals. Curcumin studies have reported effects involving caspase activation, Bax, Bcl-2, mitochondrial signaling, reactive oxygen species, NF-κB and PI3K/AKT survival pathways.
NCI’s review of laboratory research specifically identifies activation of caspases and down-regulation of anti-apoptotic gene products among the major cancer pathways influenced by curcumin.1
Apoptosis, inflammatory signaling and treatment sensitivity are central themes in curcumin cancer research.
NF-ΚB SIGNALING
One molecular target appears repeatedly in curcumin research: NF-κB.
NF-κB is a transcription factor involved in inflammation, cell survival, proliferation and resistance to apoptosis. Persistent NF-κB activity has been observed in many cancer models.
In human multiple-myeloma cells, Bharti and colleagues reported that curcumin downregulated NF-κB activity, suppressed proliferation and induced apoptosis.2
This is important because NF-κB sits at the intersection of chronic inflammatory signaling and tumor-cell survival.
STAT3 & STEMNESS
Cancer stem cells are specialized tumor-cell populations associated with self-renewal, recurrence, metastasis and treatment resistance.
Curcumin has demonstrated activity against cancer stem-like populations in several experimental systems.
In lung cancer stem-like cells, researchers found that curcumin inhibited JAK2 activity and reduced tumor-sphere formation, linking the effect to suppression of the JAK2/STAT3 pathway.3
In breast cancer cells, curcumin reduced tumor-sphere formation and decreased markers including CD44, ALDH1A1, Nanog and Oct4 while suppressing Sonic Hedgehog and Wnt/β-catenin signaling.4
COMBINATION THERAPY
One of the most clinically interesting areas of curcumin cancer research involves chemotherapy.
Instead of asking only whether curcumin affects cancer cells by itself, investigators have examined whether curcumin can make tumor cells more responsive to chemotherapy. This is known as chemosensitization.
Curcumin has been investigated alongside FOLFOX, gemcitabine, docetaxel, melphalan, prednisone and other anticancer medications. Mechanisms under study include NF-κB suppression, apoptosis, cancer stem-cell signaling, inflammatory pathways and treatment-resistance biology.
FOLFOX RESEARCH
One of the most important human studies evaluated curcumin together with FOLFOX chemotherapy, a regimen that includes 5-fluorouracil, leucovorin and oxaliplatin.
Early dose-escalation work in patients with colorectal cancer and liver metastases found that curcumin could be administered with FOLFOX at doses up to 2 grams daily.5
In a later randomized Phase IIa study, investigators compared FOLFOX alone with FOLFOX plus curcumin, referred to as CUFOX. The trial reported median progression-free survival of 320 days with CUFOX compared with 171 days with FOLFOX alone, and median overall survival of 596 days with CUFOX compared with 200 days with FOLFOX alone.6
PANCREATIC CANCER
Pancreatic cancer has been another major focus of human curcumin research.
A prospective Phase II study enrolled patients with locally advanced or metastatic pancreatic cancer who received gemcitabine together with a phospholipid-complexed curcumin formulation.7
The study reported partial responses in 27.3% of patients, stable disease in 34.1%, and an overall disease-control rate of 61.4%. Median overall survival was 10.2 months, and median time to progression was 8.4 months.7
PANCREATIC CANCER HUMAN TRIAL
Curcumin has also been studied as an oral intervention in advanced pancreatic cancer.
In an MD Anderson Phase II trial, patients with advanced pancreatic cancer received 8 grams daily of an oral curcuminoid product.8
Among evaluable patients, one experienced stable disease lasting more than 18 months, and another demonstrated measurable tumor regression. The investigators concluded that orally administered curcumin demonstrated biological activity in some patients with pancreatic cancer.8
BREAST CANCER
Curcumin has also been studied directly alongside docetaxel chemotherapy in women with advanced or metastatic breast cancer.
A French Phase I dose-escalation trial evaluated curcumin with docetaxel.9
Among evaluable patients, five experienced partial responses and three experienced stable disease. The investigators established a recommended curcumin dose of 6 grams daily for seven consecutive days every three weeks for future study with docetaxel.9
MULTIPLE MYELOMA
Multiple myeloma has generated especially interesting curcumin research because NF-κB plays an important role in myeloma biology.
A randomized study evaluated curcumin as an adjunct to melphalan and prednisone in multiple-myeloma patients.10
The investigators reported an overall remission rate of 75% in the curcumin group compared with 33.3% in the control group. The curcumin group also demonstrated reductions in NF-κB, VEGF and TNF-α.10
ANGIOGENESIS & INVASION
A growing tumor requires access to blood vessels. The process through which tumors stimulate new blood-vessel formation is called angiogenesis, and one of the central mediators is VEGF.
NCI includes VEGF-mediated angiogenesis among the major cancer pathways affected by curcumin in preclinical research.1
Curcumin has also been studied in relation to MMP-9, adhesion molecules and CXCR4—pathways involved in tumor invasion, tissue remodeling and metastasis.1
RADIATION RESPONSE
Curcumin has also been investigated as a radiosensitizer, meaning a compound that may increase the responsiveness of cancer cells to radiation.
An influential study using PC-3 prostate cancer cells found that curcumin conferred a radiosensitizing effect, increasing radiation-induced growth inhibition and apoptosis.11
Human research has also evaluated curcumin during prostate radiotherapy. In a randomized trial, 40 prostate cancer patients undergoing radiation received curcumin or placebo, and researchers evaluated oxidative status before and after radiation.12
INFLAMMATION & QUALITY OF LIFE
Chronic inflammatory signaling is closely connected with cancer biology.
Curcumin has been extensively studied for its influence on NF-κB, TNF-α, IL-1, IL-6, IL-8, COX-2 and related inflammatory systems.1
A randomized double-blind trial in patients with solid tumors evaluated a bioavailability-boosted curcuminoid formulation and reported suppression of systemic inflammation along with improvements in quality-of-life measures.13
METABOLIC ONCOLOGY
Cancer cells alter the way they generate and use energy. Modern curcumin research increasingly examines metabolic systems involving glucose utilization, lipid metabolism, mitochondrial activity and redox signaling.
Metabolomics research in breast cancer cells treated with curcumin, including curcumin with docetaxel, identified changes involving glutathione metabolism, lipid metabolism and glucose utilization.14
These findings add another dimension to the relationship between curcumin and cancer, positioning curcumin as a compound that may influence inflammatory, apoptotic and metabolic pathways simultaneously.
FORMULATION MATTERS
One of the most active areas of curcumin research involves formulation.
Researchers have studied standard curcuminoid extracts, micronized curcumin, phospholipid complexes, phytosome formulations, micellar formulations, nanocurcumin and other enhanced-delivery systems.
NCI notes that clinical pharmacology studies have detected curcumin and curcumin conjugates in plasma, urine and tissue following different formulations.1
This matters because turmeric powder, ordinary curcumin extracts and enhanced-delivery curcumin formulations are not pharmacologically identical.
HUMAN COLORECTAL TISSUE
Human pharmacology research has directly evaluated curcumin inside colorectal tissue.
Clinical studies in colorectal cancer patients have detected curcumin and related metabolites in colorectal tissue after oral administration. NCI’s review includes several clinical pharmacology studies demonstrating tissue exposure and measurable pharmacodynamic effects in colorectal cancer patients.1
One clinical study also reported increased p53 expression in patients with colorectal cancer after curcumin administration.15
PHYSICIAN-DIRECTED INTEGRATIVE ONCOLOGY
At Sunridge Medical, natural compounds are not approached simply as over-the-counter supplements. The objective is to consider them within an individualized cancer-treatment strategy.
For a patient receiving chemotherapy, radiation therapy, immunotherapy, targeted therapy, hormonal therapy or another physician-directed treatment, curcumin may be evaluated in the context of:
Curcumin is particularly compelling within integrative oncology because much of the published research focuses on treatment sensitivity, apoptosis, inflammation, cancer stem cells and combination therapy.
FREQUENTLY ASKED QUESTIONS
Laboratory research has reported effects on apoptosis, NF-κB, STAT3, PI3K/AKT, cell-cycle proteins, VEGF, MMP-9, CXCR4 and multiple inflammatory pathways.
Yes. Apoptosis is one of the major mechanisms studied in curcumin cancer research. Investigators have observed caspase activation, changes in pro- and anti-apoptotic proteins and mitochondrial death signaling.
Multiple studies have demonstrated effects on cancer stem-like populations. Lung cancer research has identified JAK2/STAT3 signaling, while breast cancer research has implicated Wnt/β-catenin and Hedgehog pathways.
Yes. Human clinical studies have evaluated curcumin with FOLFOX, gemcitabine, docetaxel, melphalan/prednisone and other cancer treatments.
Yes. A randomized Phase IIa colorectal cancer trial compared FOLFOX with FOLFOX plus curcumin. The small study reported longer median progression-free and overall survival in the CUFOX group.
Yes. A prospective Phase II pancreatic cancer trial evaluated gemcitabine plus a phospholipid-complexed curcumin formulation and reported a 61.4% disease-control rate.
Yes. Laboratory research has demonstrated radiosensitizing effects, and randomized human research has evaluated curcumin during prostate radiotherapy.
Sunridge Medical is located in Scottsdale, Arizona, and works with patients seeking physician-directed integrative cancer treatment from Arizona, throughout the United States and internationally.
BECOME A PATIENT
Curcumin research spans apoptosis, cancer stem cells, inflammatory signaling, FOLFOX, gemcitabine, docetaxel, radiation response, tumor metabolism and human clinical studies.
Call our Patient Care Team to discuss integrative cancer treatment at Sunridge Medical in Scottsdale, Arizona.
RESEARCH REFERENCES
Browse 78 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.
Finally, AKT, MMP14, E-cadherin and N-cadherin were analyzed by Western blot assay to confirm whether curcumin could inhibit bladder cancer by inhibiting invasion via AKT/MMP14 pathway.
Experimental analyses revealed that PSMG1 was markedly upregulated in bladder cancer (BCa), progressively upregulated from normal tissue to MIBC, and PSMG1 silencing reduced cell proliferation, invasion, and clonogenic capacity in vitro, while attenuating tumor growth in vivo.
Curcumin (CUR)-with antioxidant and anti-cancer properties-downregulates Hh components in cancer, inhibiting progression.
The results showed that curcumin effectively decreased cell viability and increased apoptosis rate.
Furthermore, the level of proteins related to angiogenesis and Wnt pathway-associated genes in the nanomicelle-curcumin + erlotinib group were significantly decreased compared to the curcumin, erlotinib, and control groups.
Preclinical studies have demonstrated the efficacy of curcumin analogs, including C-150, ALZ003, and DMC-BH, in inhibiting GBM growth, angiogenesis, and improving survival in orthotopic and xenograft mouse models.
Estimated survival characteristics demonstrated that the nanogel could play a significant role in TMZ-resistant tumor inhibition with low drug-induced toxicity.
In conclusion, we have shown that nano micelles curcumin effectively prevent proliferation, and invasion of GBM cells through perturbation of Wnt/β-catenin and NF-κB pathways, suggesting further investigations on the therapeutic application of this novel anticancer drug in in vivo models.
The obtained results showed that all treatments of Apatinib, Curcumin, and Apa-Cur significantly decreased viability and proliferation of the breast cancer cells in a concentration- and time-dependent manner.
Modern pharmacological studies have found that curcumin has many kinds of pharmacological activities of anti-inflammatory, anti-tumor, anti-angiogenesis, anti-metastasis and anti-multidrug resistance.
Curcumin (20 and 30 μM) inhibited the proliferation, migration and invasion, and promoted the apoptosis of MCF-7 and MDA-MB-231 cells.
Curcumin (CUR) is a well-known natural compound, which exhibits excellent anti-cancer potential by regulating many proliferative, oncogenic, and chemo-resistance associated genes/proteins.
Moreover, in vivo experiments showed that a combination curcumin and gemcitabine significantly reduced tumor size, tumor growth rate and LAT2 expression in a gemcitabine-resistant CCA xenograft mouse model.
Curcumin has therapeutic potential with various anticancer properties.
In conclusion, turmeric spice and curcumin may affect the metabolomics of probiotics in intestinal flora which could subsequently influence their anticancer properties.
Deletion of miR-34a and miR-34b/c significantly reduced curcumin-induced apoptosis and senescence, and prevented the inhibition of migration and invasion by curcumin or ectopic NRF2.
Curcumin significantly reduced CRC cell viability, migration and invasion in a dose‑dependent manner.
Curcumin significantly accelerated cell apoptosis, and inhibited cell proliferation and invasion in LoVo and HCT-116 cells.
Curcumin reduced the MACC1 expression, restricted the MACC1-induced proliferation, and was able to reduce the MACC1-induced cell motility as one of the crucial steps for the distant dissemination of the tumor.
DMC-BH, a curcumin analog, has been reported to possess anticancer properties against human gliomas.
Curcumin (CUR), a natural phenolic compound, has been increasingly investigated in several malignancies due to its safe profile and ability to affect a wide range of oncogenic targets.
Additionally, ESCC cells exposed to 20 μM of curcumin exhibited significantly decreased proliferative and invasive capacities, as well as enhanced cell apoptosis.
In contrast to concerns that curcuminoids taken by patients through diet or diet supplements might interfere with chemotherapy, suppression of 5-FU efficacy by curcumin was not observed.
These results suggest that GL63 has more potent antitumor activity than curcumin, which is associated with activation of ER stress, induction of G2/M arrest and apoptosis in NPC cells.
Inhibition of Poly (ADP-ribose) Polymerases (PARP) results in the blocking of DNA repair cascades that eventually leads to apoptosis and cancer cell death.
Curcumin synergized DTX showed significantly greater reduction in tumor burden than either treatment alone via down-regulation of MDSCs, M2 macrophages and up-regulation of CD8+ T cells, NK cells, M1 macrophages.
Curcumin suppresses proliferation, migration, invasion, metastasis and angiogenesis and induces apoptosis by regulating multiple signalling pathways and miRNAs in a wide variety of human malignancies. miRNAs play crucial roles in various steps of carcinogenesis in nasopharyngeal carcinoma (NPC); thus, they could serve as critical therapeutic targets for NPC treatment.
Curcumin treatment significantly inhibited the proliferation and invasion of C6661-IR cells, promoted apoptosis and enhanced radiosensitivity.
In conclusion, the results of the present study demonstrated that curcumin was able to reverse HGF-induced EMT, possibly by inhibiting c-Met expression in oral cancer cells, providing a strong basis for the development of novel approaches for the treatment of oral cancer.
Our results showed that curcumin inhibited SCC-25 cells proliferation and induced G2/M phase arrest in a dose-dependent manner.
Curcumin was applied as a noninvasive topical paste to the tumors and inhibition of tumor growth was observed in xenografts from the CAL27 cell line.
Curcumin (Cur) is a natural polyphenol that exhibits potent anti-tumor properties; however, the underlying molecular mechanisms regarding cell death modalities in HNSCC remain underexplored.
Comparative analyses of three anti-cancer natural products, including curcumin, gingerol, and allicin, revealed that only curcumin robustly inhibited HNSCC cell proliferation, invasion, and cancer stem cell self-renewal, with potency comparable or superior to cisplatin.
This multimodal mechanism significantly inhibited primary tumor growth and metastasis in HNC models, while extending survival.
In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effects of curcumin is unclear.
In tumor-bearing mice the combination regimen showed a decrease in both tumor weight (25%, P = .09) and tumor size (15%, P = .23) compared to the nontreated mice. : Curcumin inhibited HNSCC cell growth and augmented the effect of radiation in vitro and in vivo.
Curcumin treatment in micromolar concentration (0-50 μM) demonstrated significant differential inhibition in CSC proliferation, orosphere formation and miRNA-21 expression in a dose dependent manner, the effect being highly pronounced in HPV positive CSCs.
The results exhibited that cell viability reduced following curcumin treatment in a concentration- dependent manner.
This study explored the optimization of poly(lactic-co-glycolic acid) nanoparticles co-loaded with Er and Cm (Er/Cm-NP), prepared via a D-optimal response surface design-guided nanoprecipitation process.
Curcumin, a naturally occurring bioactive compounds, has gained increasing attention for its potential anticancer properties.
When combining these curcumin concentrations with UVA or visible light irradiation cell proliferation as well as development of reactive oxygen species was reduced whereas DNA fragmentation was increased.
5-Fluorouracil and curcumin synergistically induced apoptosis and cell cycle arrest in Hep-2 cells.
Celastrol and curcumin, both derived from traditional Chinese medicine, have demonstrated antitumor potential.
Curcumin could inhibit VM formation by suppressing ETS-1, VE-Cadherin, and MMP9 expression both in vitro and in vivo.
The results demonstrated that curcumin and tetrahydrocurcumin induced cell death by apoptosis and autophagy, respectively, in Ara-C-resistant HL60 cells.
Furthermore, curcumin suppressed proliferation and promoted apoptosis of HL-60/ADR cells.
Overall, our results suggest that curcumin potentiates TRAIL-induced apoptosis through modulation of death receptors and anti-apoptotic proteins which significantly enhances the therapeutic efficacy.
Curcumin treatment sensitized response to Ara-C in MNCs of AML mice, but had no direct effect on AML cell lines.
Therefore, curcumin exerts anti-cancer effects by inhibiting cell proliferation and promoting cell apoptosis in HCC.
Curcumin administration (100 mg/kg for 15 days) markedly suppressed tumor growth, reduced glutathione levels in tumor tissues, and enhanced the accumulation of reactive oxygen species, malondialdehyde, and Fe2+.In vitro, curcumin inhibited HepG2 cell proliferation, promoted ferroptotic cell death, downregulated P62 and NRF2 expression, and upregulated KEAP1 expression.
Curcumin (CUR) as one of the natural edible pigments is approved by the World Health Organization due to its nontoxic and anticancer effect.
Curcumin reduced LC cell proliferation, metastasis, and accelerate apoptosis, while circRUNX1 overexpression reversed these effects.
Curcumin inhibited proliferation of CA46 cells in a time- and dose-dependent manner, 2.
Further, combination of DOX with other anticancer drugs, such as curcumin, can enhance the synergistic effects, possibly through epigenetic mechanisms.
The study found that curcumin induced apoptosis in CTCL cells by activating mitochondrial signaling pathways and caspases leading to growth inhibition.
Curcumin could inhibit the proliferation, migration, and invasion of melanoma cells.
Functionally, TCPC significantly suppresses cell viability, migration, and invasion in vitro.
CCK-8 was used to detect curcumin and derivative IC50, crystalline violet staining was used to detect the proliferation inhibition effect of NL01 in ovarian cancer, western blot and qPCR were used to detect downstream related molecular expression changes, Transwell and survival curve assays were used to detect malignant phenotypic.
Our results demonstrated that curcumin inhibited proliferation, migration, and invasion of SK-OV-3 and A2780 cells in a dose-dependent manner, while inducing apoptosis and ferroptosis, as evidenced by elevated reactive oxygen species (ROS), MDA, Fe2+ levels, and depletion of GSH.
Circ-PLEKHM3 overexpression exacerbated the effect of curcumin on ovarian cancer cell proliferation and apoptosis, as well as anti-tumor effect.
Curcumin has been shown to effectively inhibit the proliferation and invasion of ovarian cancer cells but its bioavailability restricts its application.
The study reports rETRACTION NOTICE: Curcumin and resveratrol inhibit chemoresistance in cisplatin-resistant epithelial ovarian cancer cells via targeting P13K pathway.
Many evidence have shown the efficacy of curcumin (CUR) in inhibiting the progression of PCa.
In addition, transfection of miR-30a-5p inhibitors partially reversed the function of curcumin on cell proliferation, migration, invasion and apoptosis.
We used Annexin V-FITC/PI to quantify apoptotic cell death. qRT-PCR was also used to detect miRNA and gene expression levels after curcumin treatment.
Finally, chemotherapeutic agents and curcumin reduced the size of DU145 and PC-3 spheroids and have the potential to induce apoptosis and also in Matrigel.
Curcumin (CUR)-with antioxidant and anti-cancer properties-downregulates Hh components in cancer, inhibiting progression.
The results showed that curcumin effectively decreased cell viability and increased apoptosis rate.
Synthetic analogues of curcumin have elicited potent anti-cancer activity in multiple in vitro and in vivo models of human cancer.
Curcumin dose-dependently induced apoptosis of NTera-2 cells by reducing FasL expression and Bcl-2-to-Bax ratio, and activating caspase-9, -8 and -3.
Curcumin, bleomycin, and H2O2 caused apoptosis indicated as increases in caspase-3, caspase-8, and caspase-9 activities and Bax and cytoplasmic Cyt-c levels and a decrease in Bcl-2 level.
Curcumin significantly decreased LPO, 8-isoprostane and protein carbonyl content, and TBARS levels increased in cells treated with bleomycin and H2O2.
Curcumin (20 µM), bleomycin (400 µg/ml) and H2O2 (400 µM) incubation for 24 h decreased the viability of NTera-2 cells, and increased caspase-3, -8 and -9 activities, Bax and cytoplasmic cytochrome c levels and decreased Bcl-2 levels.
In the present study, curcumin significantly inhibited the growth of thyroid cancer cells.
Tumorigenesis is significantly inhibited by curcumin.
We observed that curcumin treatment decreased B-CPAP cell proliferation and promoted apoptosis.
This anti-EMT effect was confirmed by showing PAC-dependent inhibition of the proliferation and migration abilities of ATC cells.
In vitro, LC resulted in dose-dependent inhibition of proliferation, induction of apoptosis, and suppression of Ishikawa and HEC-1 cell motility.
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