Tanshinone IIA Alleviates the Biological Characteristics of Colorectal Cancer via Activating the ROS/JNK Signaling Pathway.

Abstract

Tanshinone IIA (Tan IIA) exerts a significant inhibitory effect on various tumor cells since it induces cell apoptosis and affects the proliferation, differentiation, metastasis, and invasion of tumor cells. However, the mechanism underlying the antitumor activity of Tan IIA has not been totally elucidated. This study aimed to uncover the role of Tan IIA in colorectal cancer (CRC) and its potential mechanism of action. Cell proliferation was assessed using CCK-8 and colony formation assays. Western blot analysis was carried out to detect the expression of related proteins. Cell apoptosis was assessed using flow cytometry. Furthermore, tumor size and tumor weight of CRC xenograft mice were recorded before and after Tan IIA treatment. The production of reactive oxygen species (ROS) was measured by a ROS kit. The results revealed that Tan IIA induced autophagy and apoptosis via activating the ROS/JNK signaling pathway in CRC cells, thus inhibiting the progression of CRC in vivo. The aforementioned findings indicated that Tan IIA exerted an antiproliferative effect on CRC by inducing cell autophagy and apoptosis via activating the ROS/JNK signaling pathway. Therefore, Tan IIA may be considered a potential therapeutic agent for treating CRC.