报告题目：Non-classical roles of vitamin D and vitamin D receptor in inflammation and cancer: beyond bone
报 告 人：Jun Sun
               Associate Professor, Department of Biochemistry, Rush University, USA
报告时间：2012年11月5日上午10:00
报告地点：生物药学楼树华多功能厅
Abstract：Current research has implicated vitamin D deficiency as a critical factor in the pathology of at least 17 varieties of cancer. Vitamin D exerts its role via vitamin D receptor (VDR). In particular, we note a consistent link between low vitamin D/VDR signaling and high intestinal inflammation: (i) low VDR expression and diminished vitamin D/VDR signaling are observed in patients with inflammatory bowel disease and colon cancer; (ii) vitamin D/VDR signaling regulates immune responses, a key factor in cancer etiology; and (iii) low VDR status potentiates the development of cancer. We hypothesize that VDR is required for intestinal epithelium functions and inhibition of inflammation and tumorigenesis. We found that cells lacking VDR are in a pre-inflammatory state. Overexpression of VDR substantially reduced inflammation in VDR-/- cells. Using whole body VDR knockout mice and intestinal epithelial VDR conditional knockout mice, we found that mice lacking VDR are more susceptible to Salmonella-colitis and colon cancer. Delineating the mechanisms that regulate intestinal VDR signaling will help us understand how to modulate VDR signaling so as to restore normal functioning of VDR in chronic diseases.