肿瘤休眠细胞的存在是卵巢癌化疗耐药及复发的主要原因，其机制仍未阐明。我们的前期研究发现，沉默MED12能下调EGFR的表达，诱导卵巢癌细胞进入休眠状态。本研究拟采用免疫组化及基因测序技术检测卵巢癌标本中MED12的表达水平及基因突变状态，分析MED12的表达水平及突变状态与卵巢癌化疗效果及复发的关系；以CRISPR-Cas9或基因转染技术沉默或过表达MED12，研究其对卵巢癌细胞休眠和耐药的影响；通过裸鼠移植瘤模型，研究MED12在体内调控卵巢癌休眠的作用；通过mRNA芯片及ChIP-seq等方法，探索MED12调控的候选靶基因；以ChIP、双荧光素酶报告基因等分子生物学方法，研究MED12调控EGFR及其下游信号通路的分子机理。本研究将揭示MED12在卵巢癌中的表达、突变及调控规律，阐明MED12调控卵巢癌休眠的作用及其分子机理，为卵巢癌治疗提供新思路，为克服卵巢癌耐药、复发提供新策略。

The high recurrence rate and chemoresistance of ovarian cancer are attributed to the emergence of tumor dormancy cells that are refractory to chemotherapy and clonally develop into recurrent tumors. The mechanisms underlying tumor dormancy have been elusive and not well characterized. In preliminary study, our group found that loss of MED12 could down-regulate EGFR to induce tumor dormancy in ovarian cancer cells. In this study, we will examine the expression level and mutation of MED12 by immunohistochemistry and gene sequencing to investigate the clinical significance of MED12 in ovarian cancer. CRISPR-Cas9 and transfection will be used to study the function of MED12 in tumor dormancy and chemoresistance of ovarian cancer in vitro. Xenografts in nude mice will be used to study the function of MED12 in tumor dormancy in vivo. Identification of downstream target genes of MED12 will be performed by microarray analysis and ChIP-seq assay. The mechanism of regulation of EGFR and downstream signaling by MED12 will be studied by ChIP, luciferase and other techniques. The study aims to investigate the effects of MED12 on tumor dormancy and its clinical significance in human ovarian cancer, to illustrate the function and mechanism of MED12 in regulating tumor dormancy, and to provide new strategies to overcome recurrence of ovarian cancer.