Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
Every entry includes the original study title, year, concise finding and a direct PubMed link.
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Start with the page that best matches the primary site. Each page returns here for the broader, searchable Head & Neck Cancer research collection.
Browse 81 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
In clinic, the berberine (BBR) compound has widely been in NPC therapy to decrease metastasis and disease recurrence, and BBR was documented as a main component with multiple anti-NPC effects.
Our primary studies showed that berberine induced apoptosis in human tongue cancer SCC-4 cells in vitro.
Male nude mice inoculated subcutaneously with CNE-2 cells were used to examine the sensitizing effects of berberine in vivo.
Our results showed that treatment with berberine reduced the proliferation and viability of CNE-2 cells in a dose- and time‑dependent manner.
In the present study, we investigated berberine‑induced apoptosis and the signaling pathways underlying its activity in FaDu head and neck squamous cell carcinoma cells.
Here, we showed that BBR exerted its anti-metastasis role by inhibiting system Xc-/GSH/GPX4 axis-driven ferroptosis.
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.
Herein, the study showed that EGCG could significantly inhibit cell proliferation and promote apoptosis of 2 NPC (CNE-2 and 5-8F) cell lines.
The DiOC6 (3) negative cell rate was increased and p65 of NF-κB, XIAP and survivin expression was reduced by the combination treatment.In summary, EGCG sensitizes NPC cells to TRAIL-mediated apoptosis via modulation of extrinsic and intrinsic apoptotic pathways and inhibition of NF-κB activation.
The results revealed that EGCG considerably inhibited the migration abilities of three NPC cells.
G-Rh2 significantly inhibited oral cancer cell growth by inducing apoptosis and cell cycle G0/G1-phase arrest.
In addition, we demonstrated that ginsenoside M1 dose-dependently inhibited the colony formation and migration ability of SAS and OEC-M1 cells and reduced the expression of metastasis-related protein vimentin.
Ginsenoside Rd inhibits tongue cancer cell migration and invasion via the H19/miR-675-5p/CDH1 axis.
Ginsenoside Rg3 (Rg3), an active pharmaceutical component extracted from traditional Chinese medicine ginseng, shows antitumor effects in various cancers.
This study aimed to elucidate the role of glutathione peroxidase 4 (GPX4) on the sterol regulatory element binding proteins (SREBPs)-proliferation pathway in oral cancer cells, and determine its protein expression in oral cancer tissues.
Ivermectin (IVM), an antiparasitic agent with emerging anticancer properties, may enhance DOX efficacy.
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.
Melatonin, the primary hormone produced by the pineal gland, is intensely assessed for its anticancer properties.
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].
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.
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.
Our results indicated that melatonin, at pharmacological concentrations, significantly suppresses cell proliferation in a dose- and time-dependent manner.
We found that melatonin treatment significantly reduced the viability and colony formation ability of SCC-25 cells, impairing cell migration and invasion.
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.
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.
Overall, The beneficial roles of melatonin in retarding OSCC metastasis were implicated with inhibition of TANs.
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.
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.
Y33 (Lactiplantibacillus plantarum) exhibited the strongest probiotic potential, surpassing conventional anti-cancer drugs, suggesting its therapeutic potential for preventing oral cancer cell proliferation and improving survival rates in oral cancer patients.
Oral microbiome dysbiosis was found in HNSCC patients.
Hypoxia is a modifiable factor associated with poor radiation response.
To evaluate whether intratumoral bacterial load and diversity are associated with survival outcomes in head and neck squamous cell carcinoma (HNSCC) and to examine their relationship with human papillomavirus (HPV) status.
A bioinformatic analysis is a promising approach to understand the relationship between the vast tumor microbiome and cancer development.
We identified microbes in HNSCC tumor samples significantly associated with survival.
Concurrently, clinicopathologic data, survival outcomes and the incidence and grading of CRT-emergent adverse events were documented in all patients.
Our immune-related microbiome (IRM) model outperformed the TNM staging model in predicting survival, linking higher IRM model scores with poorer prognosis, and demonstrating clinical utility over TNM staging.
The samples were binned into community types using Dirichlet multinomial models, and survival outcomes were assessed by community type.
When the prognosis of groups with rates over and under the median for each microbe at the genus level was examined, rates for Leptotrichia which were over the median correlated with significantly higher overall survival rates.
The microbiome may significantly influence the effectiveness of oncological treatment, especially radiotherapy, and may also be modified by the toxic response to radiation.
It was concluded that the growth inhibition of quercetin was highly related to cell cycle arrest at the G(2)/M phase and induction of caspase-dependent apoptosis in human nasopharyngeal carcinoma HEN1 cells.
Quercetin induced a Ca2+ response in HNSCC cells, which was significantly reduced by LF1 and YM.
Quercetin has been reported to be a modulator of proliferation and survival in various types of cancers due to its cytotoxic effects.
showed that quercetin suppressed cell viability, migration, invasion and abundances of metalloproteinase-9 (MMP-9) and MMP-2 in oral cancer cells. miR-16 was down-regulated and reversed by addition of quercetin.
Quercetin (Qu) is a principal flavonoid compound and an excellent free-radical-scavenging antioxidant that promotes apoptosis.
Rapamycin treatment significantly inhibited OSCC cell proliferation and migration, increased apoptotic cell death, and upregulated cell surface expression of several immune accessory and adhesion molecules, including CD40, CD83, PD-L1, PD-L2, MHC class I, P-selectin, and VCAM-1.
Our results show that rapamycin has a selective effect at a low dose on cancer cell growth/survival.
Resveratrol (Res) is a natural phytoestrogen with antitumor activity.
Resveratrol increases cytotoxic activity in the PE/CA-PJ15 cell line and reduces cell migration capacity, while the combination of resveratrol and irradiation exerts a synergic effect.
Resveratrol inhibited the adhesion, migration, and invasion of OSCC cells in vitro, suggesting that it might serve as a chemopreventive agent for reducing the invasion and metastasis of OSCC.
Resveratrol treatment of CAL-27 cells showed that several lines of apoptotic manifestation and decreased cell migration, invasion, and EMT-inducing transcription factor.
CCK-8, scratch wound, and transwell assays were employed to confirm the inhibitory effect of resveratrol on the proliferation, migration, and invasion of nasopharyngeal carcinoma cells.
It was strongly suggested that resveratrol-induced autophagy resulted from the inhibition of SREBP1-mediated cell survival signaling.
We first differentiated quiescent human fibroblasts into CAFs in vitro in response to PDGF-B and TGF-β stimulation and these CAFs were found to increase CXCL-12 and IL-6 secretion.
Resveratrol downregulated angiogenin, VEGF, RGS5, CD105, and the cell adhesion molecules ITGA5, ITGB1, and CD44 expressions to inhibit the vascular normalization, metastasis, adhesion, and migration of CAL-27 cells.
Dose-response curves of etoposide and resveratrol in three HNSCC cell lines were generated.
Resveratrol, in a dose-dependent manner, inhibited proliferation related proteins (Ki67, PCNA), and cell proliferation, and reduced apoptosis related proteins (cleaved caspase-3, cleaved caspase-9) and apoptosis in nasopharyngeal carcinoma cells.
Notably, we provide evidence that resveratrol (REV) strongly inhibits RCP-induced Zeb1 expression through blocking β1 integrin endosome recycling and EGFR activation, leading to suppression of RCP-induced OSCC invasion, demonstrating the important role of RCP in OSCC invasion and its reversion by REV.
Compared with vehicle, sulforaphane significantly reduced the incidence and size of 4NQO-induced tongue tumors in mice.
Cell proliferation and HDAC activity (44% in 24 h and 40% in 48 h) were significantly inhibited (p < 0.01).
Sulforaphane has been demonstrated to exert numerous biological effects, such as neuroprotective, anti-inflammatory, and anticancer effects.
Sulforaphane-cysteine (SFN-Cys) is a naturally-occurring form of plant-derived isothiocyanate metabolites that displays several tumor-suppressive properties.
The VDR, a member of the nuclear receptor superfamily, is activated by its ligand vitamin D (VitD) and analogs, triggering multiple cellular responses.
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