Molecular Studies on MIC1/PDF in Human Prostate Cancer
Annual rept. 1 Sep 2004-31 Aug 2005
NEBRASKA UNIV MEDICAL CENTER OMAHA
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The overall objective of this proposal is to investigate the incidence, function and regulatory mechanisms of a highly expressed MIC-1PDF gene in prostatic cancer cells. We and other groups have observed that the macrophage inhibitory factorprostate derived factor MIC-1PDF is overexpressed during the progression of numerous cancer types including prostate cancer, few studies on oncogenic signaling cascades which might be involved in the regulation of this expression have yet been reported 1-6. Moreover, the mechanism of action of MIC-1 which appear to be dependent of cancer cell types is yet controversial 4,6. This is in part due to lack of information about the MIC-1 receptor or binding sites and intracellular signaling elements activated by this pleiotropic factor in cancer cells during prostate carcinogenesis. Therefore, this supports the importance of our work to further characterize the implication of MIC-1 expression and secretion in malignant transformation of prostatic epithelial cells.
- Medicine and Medical Research