Hinokitiol Inhibits the Viability of Oral Squamous Carcinoma Cells by Inducing Apoptosis and Autophagy

Background/Aim: Oral squamous cell carcinoma (OSCC) is one of the deadliest cancers, with approximately similar to 500,000 new diagnosed cases and 145,000 deaths worldwide, per year. The incidence of new cases continues to increase in developing countries. This study aimed to investigate the effect of hinokitiol on cell viability in OSCC cells. Materials and Methods: The anticancer effect and mechanism of action of hinokitiol in OSCC cells were analyzed by cell viability assays and cell cycle analysis using flow cytometry, while apoptosis and autophagy-related protein expression was measured using western blot. Results: The results showed that hinokitiol concentration -dependently reduced the viability of SCC4 and SCC25 cells by downregulating the levels of cell-cycle mediators, such as cyclin B1, cyclin D1 and cyclin-dependent kinase-1 (CDK1). Furthermore, hinokitiol promoted apoptosis in SCC25 cells based on the presence of active cleaved caspase-3. Hinokitiol also induced autophagy by promoting the accumulation of the microtubule-associated protein light chain 3B (LC3B) and the expression of the sequestosome-1 (p62/SQSTM). Conclusion: Hinokitiol exhibits anti -proliferation activity and has pro-apoptotic effects on OSCC cell lines.

Automated summary

This study aimed to investigate the effect of hinokitiol on cell viability in oral squamous cell carcinoma (OSCC) cells. The results showed that hinokitiol can downregulate the levels of cell-cycle mediators, reduce cell viability, promote apoptosis, and induce autophagy in OSCC cell lines.