目的通过检测桥粒胶蛋白-3(Dsc3)在卵巢癌中的表达以及促卵泡激素(FSH)对Dsc3、EGFR/Akt信号通路下游分子以及细胞增殖的影响,探讨Dsc3是否介导FSH通过EGFR/Akt信号通路对卵巢癌细胞增殖活性的调控,进而促进肿瘤的发生。方法免疫组化检测Dsc3在卵巢肿瘤组织中的表达;运用蛋白质印迹分析方法检测Dsc3在6种卵巢肿瘤细胞及卵巢永生化上皮细胞中的表达情况和FSH对Dsc3、EGFR的调控,以及干扰Dsc3、EGFR和应用Akt通路阻断剂对信号通路分子的调控;运用MTT方法检测干扰Dsc3、EGFR以及使用Akt阻断剂后对卵巢癌细胞增殖活性的影响。结果 (1)Dsc3在卵巢癌及交界性卵巢肿瘤中的阳性表达率均高于良性卵巢肿瘤,差异均有统计学意义(P<0.05),Dsc3在卵巢癌中的阳性表达率与交界性卵巢肿瘤的差异无统计学意义(P>0.05);Dsc3在某些卵巢癌细胞如Hey、HO8910中及交界性卵巢肿瘤细胞MCV152中的表达高于卵巢永生化上皮细胞Moody;(2)FSH呈剂量-时间依赖效应上调Dsc3、EGFR的表达;(3)干扰Dsc3后,信号通路分子EGFR、pAkt受到抑制,Akt无明显改变;干扰EGFR后,信号通路分子Dsc3、pAkt受到抑制,Akt无明显改变;应用Akt通路阻断剂后,Dsc3、pAkt受到抑制,Akt无明显改变;以上三种处理均可抑制FSH对Akt信号通路的调控;(4)干扰Dsc3、EGFR,及应用Akt通路阻断剂均可抑制FSH介导的卵巢癌细胞增殖活性(P<0.05)。结论 Dsc3介导FSH通过EGFR/Akt通路调控的卵巢癌细胞增殖活性,进而促进卵巢癌的发展。 OBJECTIVE: To investigate whether Dsc3 mediates the expression of FSH through EGFR / Akt pathway by detecting the expression of desmosome-3 (Dsc3) in ovarian cancer and the effects of follicle stimulating hormone (FSH) on the downstream molecules and cell proliferation of Dsc3 and EGFR / Akt signaling pathway, Akt signaling pathway on ovarian cancer cell proliferation and regulation, thereby promoting the occurrence of tumors. Methods The expression of Dsc3 in ovarian tumor was detected by immunohistochemistry. The expression of Dsc3 in 6 kinds of ovarian tumor cells and immortalized ovarian epithelial cells was detected by Western blotting, and the regulation of Dsc3 and EGFR by FSH and the interference of Dsc3, EGFR and Akt pathway blockers on the signaling pathway molecules. The effects of Dsc3, EGFR and Akt blockers on the proliferation of ovarian cancer cells were detected by MTT assay. Results (1) The positive rates of Dsc3 in ovarian and borderline ovarian tumors were significantly higher than those in benign ovarian tumors (P <0.05). The positive rate of Dsc3 in ovarian cancer and borderline ovarian (P> 0.05). The expression of Dsc3 in some ovarian cancer cells such as Hey, HO8910 and borderline ovarian tumor cell MCV152 was higher than Moody in ovarian immortalized epithelial cells. (2) FSH was in a dose-dependent manner (3) Interfere with Dsc3, EGFR and pAkt were inhibited, but there was no significant change in Akt. After interfering with EGFR, Dsc3 and pAkt were inhibited, Akt had no obvious change; Akt pathway inhibitor, Dsc3, pAkt was inhibited, Akt no significant change; the above three treatments can inhibit FSH Akt signaling pathway regulation; (4) interference Dsc3, EGFR, and application of Akt pathway blockers are Can inhibit FSH-mediated proliferation of ovarian cancer cells (P <0.05). Conclusion Dsc3 mediates the proliferative activity of FSH through EGFR / Akt pathway in ovarian cancer cells, and then promotes the development of ovarian cancer.