| Summary: | 碩士 === 長庚大學 === 醫學生物技術研究所 === 97 === The imbalance between cell proliferation and cell death leads to cancer formation. Inappropriate expression or activation of proto-oncogene or lost of tumor suppressor gene disrupts cell growth. Prostaste cancer (PrCa) is a leading cause of cancer-related death in men. According to previous studies, overexpressed of PKCε promotes survival of human prostate cancer cells through interact with Bax. PKCε acts as an oncoprotein to inhibit cell death and promote cell growth. Several studies found that Disabled-2 (DAB2) inhibits the growth of cancer cells, suggest that DAB2 acts as an tumor suppressor gene. In this study, we used prostate cancer cell line model to study the role of DAB2 in prostate cancer, and whether it acts as a tumor suppressor through influence PKCε expression. We manipulated DAB2 and PKCε expression in DU145 cells by transient transfection. By western blotting, overexpresssion of DAB2 cell have less PKCε protein expression. Our results showed that DAB2 overexpression contributes to PKCε depletion and decreases cell growth of DU145 cells.We further observed the effect of drug-sensitivity while overexpression or knockdown of DAB2 or PKCε. Our data shown that DAB2 might increase drug susceptibility through inhibiting PKC expression in DU145 cell. Taken together, these results suggest that DAB2 overexpression decreased PKCε protein expression, accompanied increase in cell growth rate and methylseleninic acid resistance. These results implicate that the level of DAB2 expression may affect the outcome of cancer chemotherapy
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