子宫内膜异位症（内异症）是妇科常见病及难治病，其发生、发展的机制一直是妇科基础与临床研究探索的重点。microRNA作为转录后调节因子，在许多生命过程中起到关键作用。本课题组在前期相关研究中发现内异症的发生与microRNA-126的低表达有关，并且发现随着microRNA-126表达的升高，子宫内膜细胞凋亡率增加，增殖、迁移及血管生成能力均下降，其原因可能与microRNA-126通过转录后调控靶基因而参与一系列信号通路从而调控细胞活动有关。本研究拟采用生物化学、免疫学及分子生物学等方法，研究microRNA-126可能通过转录后调控靶基因Crk和BCAR3影响PI3K信号通路，调节子宫内膜细胞的功能及对雌激素敏感性影响，探讨microRNA-126在内异症中作用的分子机制，证明microRNA-126在内异症发生、发展中起关键作用，为寻找内异症发生的源头分子机制及治疗靶点提供理论依据。

Endometriosis(EMs) is one of the most commonly encountered benign gynecological disorders. The pathogenesis of the establishment of EMs is the focal point of the clinical and scientific studies in gynecology. Considerable circumstantial and laboratory evidence suggests that EMs is an estrogen-dependent disease with cell functional disorders. microRNAs regulate the stability and expression of target mRNAs as essential post-transcriptional regulators that determine cell identity and fate. Since each microRNA has been predicted to have a broad range of target mRNA based on degree of sequence homology, it is estimated that changes in the expression of even a single microRNA could have a signi?cant impact on the outcome of diverse cellular activities regulated by the product of target genes..In our previous study, we found decreased microRNA-126(miR-126) expression was signi?cantly correlated with development of EMs. Our previous evidences further validate that the rate of apoptosis is up-regulated, while the ability of proliferation, migration and angiogenesis is down-regulated along with the up-regulation of miR-126. It may provide initial evidence that down-expression of miR-126 may facilitate the formation of ectopic lesions and play an important role in the development of EMs.On the other hand, in our present study, the expression of Crk protein negatively correlated with miR-126, whereas the expression of Crk mRNA was not correlated with miR-126. These results further indicate that Crk may be a target gene of miR-126, and miR-126 may play biological function in endometrium through down-regulation of Crk protein expression post-transcriptionally. It can be concluded that miR-126 are involved in molecular pathways implicated in EMs through post-transcriptional regulation on the targets, and finally control the cytolergy. .Our present studies plan to investigate that miR-126 regulate of biological behaviours of endometrial cells and the sensitivity to estrogen through PI3K signal pathway by post-transcriptional regulation of Crk and BCAR3, and first investigate the role and molecular mechanism of miR-126 in pathogenesis of EMs with the method of biochemistry, immunology and molecular biology. We may finally demonstrate that miR-126 play a primal role on development of endometriosis, and explore the origin of pathogenesis of EMs, which provide the theoretical evidence to therapeutic targets.