Resveratrol (trans-3,4,5’ –trihydroxystilbene) is an active compound in food, such as red grapes, peanuts, and berries. Resveratrol exhibits an anticancer effect on various human cancer cells. However, the mechanism of resveratrol-induced anti-cancer effect at the molecular level remains to be elucidated. In this study, the mechanism underlying the anti-cancer effect of resveratrol in human ovarian cancer cells (OVCAR-3 and Caov-3) was investigated using various molecular biology techniques, such as flow cytometry, western blotting, and RNA interference, with a major focus on the potential role of autophagy in resveratrol-induced apoptotic cell death. We demonstrated that resveratrol induced reactive oxygen species (ROS) generation, which triggers autophagy and subsequent apoptotic cell death. Resveratrol induced ATG5 expression and promoted LC3 cleavage. The apoptotic cell death induced by resveratrol was attenuated by both pharmacological and genetic inhibition of autophagy. The autophagy inhibitor chloroquine, which functions at the late stage of autophagy, significantly reduced resveratrol-induced cell death and caspase 3 activity in human ovarian cancer cells. We also demonstrated that targeting ATG5 by siRNA also suppressed resveratrol-induced apoptotic cell death. Thus, we concluded that a common pathway between autophagy and apoptosis exists in resveratrol-induced cell death in OVCAR-3 human ovarian cancer cells.

The aim of this study was to investigate the expression of cyclooxygenase type-2 (COX-2) and its association with angiogenesis and clinicopathologic characteristics of colorectal carcinoma (CRC). COX-2 expression was detected by means of immunohistochemistry in a series of human tissue samples with CRC (n = 120), dysplasia tissue closely adjacent to carcinomas (n = 40) and normal colorectal mucosa (n = 40), and their expressions association with vascular endothelial growth factor (VEGF), CD31-labeled micorvessel density(MVD) in CRC and other clinicopathologic characteristics were investigated. The expression of COX-2 in CRC tissues (78.3%) was obviously higher than that in adjacent tissue and normal mucosal tissue (p<0.01). COX-2 expression was correlated significantly with the grading, advanced cancer, Dukes stage and lymph node metastasis, distant metastasis and VEGF (p<0.05). Our result demonstrates that COX-2 expression was significantly higher in earlier stages of CRC. It can be suggested that COX-2 expression may be important in the initial development of CRC. The findings of the present study suggest that COX-2 overexpression in CRC may be considered as a negative prognostic marker.