Biography
Biography: Wei-Dong Chen
Abstract
The farnesoid X receptor (FXR) is a key metabolic and homeostatic regulator in digestion system. Our publication has shown that bile acid nuclear receptor FXR is required for the promotion of liver regeneration/repair after physical resection or liver injury, and FXR is a key negative regulator in chronic inflammation and liver carcinogenesis. We found that defective activation of FXR could be an intrinsic defect in aging regenerating livers, and other transcription factors are present as constituents of the multi-protein-DNA complex at the IR-0 element in intron 3 of Foxm1b In liver carcinogenesis, we identified a novel role of FXR in antagonizing c-Jun N-terminal kinase (JNK) signaling pathway by activating SOD3 transcription. FXR may regulate SOD3 expression to suppress ROS production, resulting in decreasing JNK activity. The results highlight FXR as a potential target for drug design for prevention and treatment of liver cancer and insufficient liver regeneration after segmental liver transplantation or resection, which may also have potential implications for treatment of other age-related diseases. In recent days, we found that FXR activation suppresses cervical cancer and ovarian cancer cell proliferation and induces cancer cell apoptosis (unpublished data). These findings identify FXR as a negative mediator not only for digestive system cancers but also reproductive system cancers that may serve as an attractive therapeutic tool for human different cancers.