Paclitaxel inhibits proliferation and promotes apoptosis through regulation ROS and endoplasmic reticulum stress in osteosarcoma cell

Molecular & Cellular Toxicology

article

Li, Ming¹  Yin, Liming¹  Wu, Lili¹  Zhu, Yunsen¹  Wang, Xi¹ 

[1] The First People’s Hospital of Wenling

关键词: Paclitaxel;    Reactive oxygen species;    COX-2;    Osteosarcoma;   

DOI  :  10.1007/s13273-020-00093-7

来源: Korean Society of Toxicogenomics and Toxicoproteomics

【 摘 要 】

Background Paclitaxel is a chemotherapeutic drug for cancer, which is isolated from the Pacific yew tree. However, and the molecular mechanism and the antitumor effects of paclitaxel on osteosarcoma cell remain to be explored. Objective The aim of our study was to explore the possible molecular mechanisms of apoptosis in osteosarcoma induced by paclitaxel. Results Paclitaxel can obviously decrease the proliferation of HOS-732 cells in a dose-dependent manner. Paclitaxel could induce the cell cycle arrest at the G2/M-phase and decreases the CDK5 and CCNE1 expression in HOS-732 cells. Paclitaxel promotes cell apoptosis in HOS-732 cells, which may be contacted to the decreasing of Bcl-2 protein expression. Further, the production of ROS in HOS-732 cells was remarkably increased with the increasing concentration of paclitaxel. Moreover, paclitaxel induces the ER-stress related gene and protein expression (GRP79, DDIT3 mRNA and GRP78, XBP-1 s, IRE1α protein expression) in osteosarcoma cells. Conclusion Paclitaxel can inhibit the proliferation of HOS-732 cells and increase ROS and ER-stress response to promote cell apoptosis, suggesting that paclitaxel may represent a new therapeutic option for the treatment and prevention osteosarcoma.

【 授权许可】

Unknown