Expressions Of Glypican-3 In Ovarian Carcinoma And Biological Function Study Of It In Ovarian Tissue

GPC3 is cloned in Simpson-Golabi-Behmel syndrome (SGBS) by Pilia in 1996. It acts as a growth suppressor during cells growth and proliferation, its mutation causes SGBS. This discorder disease includes both pre- and postnatal overgrowth, a predisposition to certain childhood carcinomas, and a complex assortment of congenital defects including visceral and skeletal abnormalities. Recent studies show it is involved in the carcinogenesis. The ectopic expression of GPC3 results in cells gowth out of control, accordingly carcinoma occurs.In order to reveal the relationship between GPC3 and ovarian carcinoma, the first part investigated the levels of GPC3 mRNA transcription and protein expression of ovarian carcinomas and discussed the clinical significance. Firstly we detected the expression of GPC3mRNA in 25 specimens of ovarian carcinomas and 23 specimens of normal ovarian tissues by real-time fluorescence quantitative RT-PCR. Result showed the expression level of GPC3 in ovarian carcinomas was lower than that of the normal ovarian tissues. The expression level of GPC3 in â…¢ â…£ grades was much lower than that in â…  â…¡ grades. Secondly we detected the expression of GPC3 protein in ovarian carcinomas and normal ovarian tissues. The expression level of GPC3 protein in ovarian carcinomas was also lower than that of the normal ovarian tissues.Biological function study of gene will be helpful to reveal the function of it in carcinogenesis. In order to discover whether GPC3 also regulates cells growth and proliferation in ovarian tissues, we incised the the primary follicles and the secondary follicles of 15 specimens of rats' ovarian tissues by laser capture microdissection (LCM) in the second part, then detected the expression levels of GPC3 in them by real-time fluorescence quantitative RT-PCR. Result showed GPC3was located at both primary follicles and secondary follicles, and the expression level of GPC3 in secondary follicles was higher than that of the primary follicles. We speculate GPC3 regulates the follicles differentiation. It is perhaps because of the ectopic expression of GPC3 results in the overgrowth of follicles' cells that the ovarian carcinoma occurs.This study showed that GPC3 might contribute to ovarian carcinogenesis and discussed the biological function of GPC3 in ovarian tissues. It provides the theoretic base for the further study of the regulating mechanism of GPC3 in ovarian carcinogenesis.