Corylin attenuates oral squamous cell carcinoma progression through c-Myc inhibition.

Background: Materials and methods: OSCC cell lines (SAS and OECM1) were treated with corylin, and its effects on cell proliferation, migration, and invasion were assessed using cell function assays. Flow cytometry and DiOC6/PI staining were performed to analyze cell cycle progression and apoptosis, while Western blotting was used to elucidate the molecular mechanisms of corylin's action. Results: Corylin selectively inhibited OSCC cell growth, migration, and invasion while exhibiting minimal toxicity toward normal human cells. Mechanistic investigations revealed that corylin downregulated c-Myc expression, which subsequently modulated the expression of cell cycle checkpoint regulators, apoptosis-related proteins, and epithelial-mesenchymal transition (EMT)-associated markers. This led to G1 phase cell cycle arrest and enhanced apoptosis induction. Additionally, corylin significantly enhanced the anticancer efficacy of cisplatin and 5-FU in OSCC cells. Conclusion: Corylin exhibits potent anticancer activity against OSCC by targeting c-Myc-mediated oncogenic pathways and may serve as a promising therapeutic candidate. Furthermore, its ability to synergize with cisplatin and 5-FU suggests its potential role in combination therapy to improve treatment efficacy.