Bavachin suppresses proliferation of laryngopharyngeal cancer by regulating the STAT3 and MAPK signaling pathways.

Abstract

Purpose: The present study aimed to explore the underlying antitumor effects of bavachin on laryngopharyngeal cancer in-vitro and in-vivo. Methods: Tu212 and FaDu cells were cultured in the incubator. Cells were treated with 0.1% DMSO (control group) and different concentrations of bavachin (experimental groups) for exploring the results of proliferation and apoptosis. We revealed the underlying mechanism of bavachin on laryngopharyngeal cancer through western blotting, qRT-PCR assay and immunofluorescence staining. Results: Bavachin could suppress the proliferation and migration of laryngopharyngeal cancer cells in-vitro and in-vivo. Mechanistically, the results suggested that bavachin could downregulate the phosphorylation level of the signal transducer and activator of the transcription 3 (STAT3) and upregulate those of the mitogen-activated protein kinase (MAPK). Furthermore, bavachin also increased the expression level of Bax and suppressed those of Bcl-2, CDK4/6, and CyclinD1 in the laryngopharyngeal cancer cells. Additionally, the study also identified that bavachin promoted ferroptosis by decreasing the expression level of glutathione peroxidase 4 (GPX4) and increasing those of intracellular reactive oxygen species (ROS) and glutathione (GSH). Conclusion: Taken together, these results demonstrated that bavachin could suppress the growth and migration of laryngopharyngeal cancer cells and induce apoptosis and cell cycle arrest of the laryngopharyngeal cancer cells by regulating the MAPK/STAT3 signaling pathway. This study demonstrated that bavachin exhibited a clinical therapeutic potential for laryngopharyngeal cancer.