Capsaicin suppresses breast cancer cell viability by regulating the CDK8/PI3K/Akt/Wnt/β-catenin signaling pathway

Breast cancer displays high morbidity and mortality. Despite exerting certain effects, traditional treatments cannot eliminate every cancer cell and may kill normal cells due to inaccurate targeting. However, as a traditional Chinese medicine, capsaicin, an active compound extracted from chili peppers, has displayed potent anticarcinogenic activities in vitro and in vivo, but the underlying mechanism is not completely understood. The pharmacological effects of capsaicin on tumors was evaluated in MDA MB 231 breast cancer cells. The MTT, cell scratch assay, cell cycle analysis, cell transfection, reverse transcription-quantitative PCR and western blotting were performed to investigate the potential antitumor mechanisms of capsaicin. In the present study, the potential anticancer mechanism underlying capsaicin in MDA-MB-231 cells in vitro was investigated. Capsaicin significantly inhibited MDA-MB-231 breast cancer cell viability and migration compared with the control group. The flow cytometry results indicated that capsaicin induced G(2)/M cell cycle arrest in MDA-MB-231 cells. In addition, capsaicin significantly reduced the expression of cyclin-dependent kinase 8 (CDK8) in breast cancer cells compared with the control group. Moreover, LV-CDK8 small interfering RNA-transduced MDA-MB-231 cells displayed lower CDK8 mRNA and protein expression levels compared with LV-negative control-shRNA-transduced cells. Furthermore, capsaicin significantly reduced the expression levels of phosphorylated (p)-PI3K, p-Akt, Wnt and β-catenin in vitro compared with the control group. Collectively, the results of the present study suggested that capsaicin inhibited breast cancer cell viability, induced G(2)/M cell cycle arrest, reduced CDK8 expression levels, decreased the phosphorylation of PI3K and Akt and downregulated Wnt and β-catenin expression levels in MDA-MB-231 cells.