Bicyclol exerts an anti-tumor effect via ROS-mediated endoplasmic reticulum stress in human renal cell carcinoma cells.

Renal cell carcinoma (RCC) is the most common subtype of kidney cancer. Currently, there is a lack of efficient treatment for RCC. Bicyclol, an anti-hepatitis drug, has been demonstrated to possess anti-tumor properties. However, the effect of bicyclol in RCC remains elusive. Therefore, the aim of this study is to investigate the biological effects of bicyclol on RCC and the underlying mechanisms. The data from this study indicated that bicyclol markedly induced cell apoptosis and cell cycle arrest and increased the production of reactive oxygen species (ROS) in RCC cells. Moreover, bicyclol induced ER stress in a ROS-dependent manner, since the ROS scavenger NAC could block this effect. Taken together, the results of this study provide evidence that bicyclol may serve as a potential therapeutic agent for the treatment of human RCC.