A new approach for pathogenesis and treatment of endometrosis using microarray analysis.

我们通过mRNA微阵列技术鉴定了丙戊酸（VPA）治疗子宫内膜异位症囊肿基质细胞（ECSCs）后组蛋白去乙酰化酶1靶mRNA的上调。我们选择CCAAT/增强子结合蛋白α (C/EBP α)进行进一步的功能实验。C/EBP α在ECSCs和子宫内膜异位症组织中的表达减弱。在ECSCs中，C/EBA α的强制表达直接抑制细胞增殖和诱导细胞凋亡。C/EBP α敲低可直接刺激正常子宫内膜细胞增殖和抗凋亡。C/EBP α α表达下调了各种生长和凋亡相关分子的表达。我们的研究结果表明，一种表观遗传抑制的肿瘤抑制基因通过创造子宫内膜异位症的增殖、抗凋亡和其他疾病特异性特征参与了子宫内膜异位症的发病机制。

We identified histone deacetylase 1-target mRNAs that were up-regulated by valpronic acid (VPA) treatment in endometriotic cyst stromal cells (ECSCs) by an mRNA microarray technique. We chose CCAAT/enhancer-binding protein alfa (C/EBP alfa) for further functional experiments. C/EBP alfa expression was attenuated in ECSCs and in endometriotic tissues. The compulsory expression of C/EBA alfa directed the inhibition of cell proliferation and the induction of apoptosis in ECSCs. C/EBP alfa knockdown directed the stimulation of cell proliferation and the resistance to apoptosis in normal endometrial cells. The expressions of various growth- and apoptosis-related molecules were down-regulated by C/EBP alfa knockdown. Our findings suggest that an epigenetically suppressed tumor suppressor gene is involved in the pathogenesis of endometriosis by creating the proliferative, anti-apoptotic, and other disease-specific characteristics of endometriosis.