Dsc3Mediates FSH-induced Ovairan Epithelial Cancer Cell Proliferation Through Activation Of The EGFR/Akt Signaling Pathway

Objective: By detecting the expression of Dsc3in ovarian cancer and the impact ofFSH on Dsc3, EGFR/Akt signaling pathway and ovarian cancer cell proliferation, toexplore whether Dsc3mediates FSH-induced ovarian epithelial cancer cell proliferationthrough activation of the EGFR/Akt signaling pathway, thereby promoting tumor.Methods: Immunohistochemical was used to detect the expression of Dsc3in ovariantumor tissues, Western blot was used to detect the expression of Dsc3in ovarian tumorcells and normal ovarian epithelial cell, and the expression of Dsc3and EGFR in proteinlevels after treatment with FSH; siRNA was used to knock down the expression of Dsc3and EGFR; After the treatment of PI3K/Akt signaling pathway inhibitor, Western blot wasused to detect the expression of Dsc3, EGFR, Akt and pAkt; MTT assay was used todetermine cellular growth.Results: Dsc3in ovarian cancer is highly expressed, and FSH in a dose-andtime-dependent manners for the expression of Dsc3and EGFR; Inhibition of Dsc3andEGFR by RNA interference and inhibition of PI3K/Akt signaling pathway could all reducethe regulation of FSH on the related factors of PI3K/Akt signaling pathway and reduceFSH-induced cell proliferation.Conclusion: Dsc3mediates FSH-induced ovarian epithelial cancer cell proliferationthrough activation of the EGFR/Akt signaling pathway, thereby promoting tumor.