子宫内膜异位症（Endometriosis，EM）严重影响妇女生育和生殖健康，现有治疗方法不能有效根治疾病、避免复发，寻找新的能有效控制EM的治疗方法刻不容缓。生长激素释放激素（GHRH）作为一种新发现的肽类激素其在肿瘤中的作用被不断证实，其拮抗剂亦在多种肿瘤的体内及体外实验中显示出良好的抗肿瘤效果。EM作为一种激素依赖性疾病，其生物学行为和肿瘤有着很多的类似之处，结合最近在子宫内膜组织及内异的细胞中GHRH及受体发现，我们推测GHRH及其受体很有可能参与EM的发生和发展，而GHRH拮抗剂MIA-602作为一种新的分子靶向治疗药物很有可能为EM的治愈带来了新的希望。我们前期实验基础上拟探究：GHRH及其受体是否参与EM的发病？MIA-602是否抑制EM异位和在位子宫内膜细胞生长？MIA-602是否通过EGFR信号通路参与调控过程？旨在揭示新的EM发病机制，为改进EM的治疗模式提供科学依据。

Endometriosis is one of the most common benign gynecologic disorders, defined as estrogen-dependent lesions containing endometrial glands and stromal outside the uterus, strongly associated with intolerable dysmenorrhea, pelvic pain and subfertility. As for today, an optimal drug does not exist that allows both, pain management as well as continuing the attempt to conceive. Therefore, it is mandatory to develop more ideal treatment strategies for endometriosis which eliminate endometriotic lesions, prevent recurrence but not impede ovulation.MIA-602 is one of the newest series of highly potent GHRH antagonists with improved design and resistance to biodegradation. It has been proven to inhibit several human experimental cancers including prostate, lung and breast cancer, but the effects on endometriosis have not been reported so far. The knowledge about the underlying signaling mechanisms of MIA-602 in endometriosis is still under investigation.Considering the importance of EGFR and its signaling pathway components in endometriosis as well as the antiproliferative function of the GHRH antagonist MIA-602 in cancer, we hypothesize that MIA-602 might inhibit the growth of human cells involved in endometriosis by interfering with the intracellular signaling pathways of EGFR/ERK1/2 and/or EGFR/Akt. Our aims for this study:.•.To identify the expressions of GHRH, pit-GHRHR and SV1 in endometrium and endometriosis tissues from women with or without endometriosis. .•.To evaluate the regulatory effects of MIA-602 on the immortalized human endometriotic epithelial cell lines. .•.To demonstrate the inhibitory mechanisms of MIA-602 on the human endometriotic epithelial cell lines by interference with the EGFR pathway.