Abstract
As a polyphenolic compound, resveratrol (Res) is widely distributed in a variety of plants. Previous studies have demonstrated that Res can inhibit various different types of tumor growth. However, its role in renal cell carcinoma (RCC) remains largely unknown. The present study first demonstrated that Res inhibited cell viability and induced apoptosis in RCC 786-O cells. Further experiments revealed that Res damaged the mitochondria and activated caspase 3. In contrast, Z-VAD-FMK, a pan-caspase inhibitor, suppressed Res-induced apoptosis. Reactive oxygen species (ROS) were involved in the process of Res-induced apoptosis, and antioxidant N-acetyl cysteine could significantly attenuate this. Furthermore, Res activated c-Jun N-terminal kinase via ROS to induce autophagy, whereas inhibition of autophagy with chloroquine or Beclin 1 small interfering RNA aggravated Res-induced apoptosis, indicating that autophagy served as a pro-survival mechanism to protect 786-O cells from Res-induced apoptosis. Therefore, a combination of Res and autophagy inhibitors could enhance the inhibitory effect of Res on RCC.