TRPM3表达上调通过调控Beclin1的表达促进卵巢癌细胞自噬

Upregulation of TRPM3 Expression Promotes the Autophagy in Ovarian Cancer Cells via Regulating Beclin1 Expression

目的:探讨瞬时受体电位离子通道3(TRPM3)和Beclin1在卵巢癌中的表达和对卵巢癌细胞自噬的影响。方法:收集6例正常卵巢组织标本和20例卵巢癌组织标本,应用免疫组织化学染色法检测TRPM3和Beclin1在卵巢癌组织中的表达,采用western blotting法检测TRPM3和Beclin1在正常卵巢上皮细胞Moody和卵巢癌细胞Hey、ES-2中的表达差异。用TRPM3-siRNA瞬时转染细胞Hey和ES-2,通过western blotting法检测TRPM3基因沉默情况及Beclin1、p62和LC3的蛋白表达变化。结果:在正常卵巢组织和卵巢癌组织中,TRPM3的阳性表达率分别为33.3%、80.0%(P<0.05),而Beclin1的阳性表达率分别为33.3%、65.0%(P>0.05)。与正常卵巢上皮细胞Moody相比,卵巢癌细胞Hey和ES-2中TRPM3、Beclin1蛋白表达水平明显较高(P<0.05)。沉默TRPM3基因表达的卵巢癌细胞中Beclin1和LC3蛋白表达与对照组相比明显降低,而p62表达升高(P<0.05)。结论:卵巢癌组织和细胞中TRPM3蛋白呈高表达,可能通过调控Beclin1促进卵巢癌细胞的自噬。

Objective： To explore the expression of transient receptor potential melastatin 3（TRPM3） and Beclin1 in ovarian cancer and their effect on the autophagy of ovarian cancer cells. Methods： 6 cases of normal ovarian tissues and 20 cases of ovarian cancer tissues were collected to detect the expression of TRPM3 and Beclin1 via immunohistochemical method. Western blotting assay was used to detect the expression of TRPM3 and Beclin1 in a human normal ovarian epithelial cell line Moody and ovarian cancer cell lines Hey, ES-2. Hey and ES-2 were transfected with TRPM3-si RNA, and western blotting assay was used to detect the silencing of TRPM3 and expression changes of Beclin1, LC3 and p62. Results： In normal ovarian tissues and ovarian cancer tissues, the positive expression rates of TRPM3 were 33.3% and 80.0%, respectively（P〈0.05）, while the positive expression rates of Beclin1 were 33.3% and 60.0%,respectively（P〈0.05）. Compared with the normal ovarian epithelial cells Moody, TRPM3 and Beclin1 protein expression levels in the ovarian cancer cells Hey and ES-2 were significantly higher（P〈0.05）. The expression of Beclin1 and LC3 were downregulated, while p62 was upregulated significantly when the expression of TRPM3 in ovarian cancer cell lines were silenced（P〈0.05）. Conclusions： TRPM3 were highly expressed in ovarian cancer tissues and cells, while TRPM3 may promote the autophagy in ovarian cancer cells by regulating Beclin1.