耐药复发是卵巢癌治疗失败的主要原因之一。我们从困扰卵巢癌临床治疗的实际出发，以卵巢癌干细胞为突破口，应用蛋白磷酸化抗体芯片技术结合生物信息学分析，发现耐药卵巢癌患者的CD44+CD117+卵巢癌细胞内存在异常激活的PIK3CA/NF-κB /STAT3信号传导通路。这一现象首次提示CD44+CD117+卵巢癌细胞内PIK3CA/NF-κB/STAT3信号传导通路调控着卵巢癌患者对化疗药物的反应。为此，本项目拟在较大样本、较长周期内进一步分析CD44+CD117+卵巢癌细胞内PIK3CA、NF-κB及STAT3的异常表达模式与卵巢癌临床特征的相关性；通过体内外实验深入探索PIK3CA/NF-κB/STAT3信号传导通路的激活机制及其对CD44+CD117+卵巢癌细胞化疗药物敏感性及干细胞特性的调控，为预测卵巢癌患者对术后化疗药物的反应性和个体化治疗提供新的理论和实验基础。

Chemoresistance and recurrence are the main reasons for the treatment failure in ovarian cancer. Because of the dilemma of treatment in ovarian cancer, selecting stem cells as the object of study and combining Phospho Explorer Antibody Array and bioinformatics, we found that PIK3CA/NF-κB/STAT3 signaling pathway in CD44+CD117+ ovarian cancer cells was abnormally activated in patients with chemoresistant ovarian cancer. This phenomenon was first suggested that PIK3CA/NF-κB/STAT3 signaling pathway in CD44+CD117+ ovarian cancer cells regulated response to chemotherapy in patients with ovarian cancer. Therefore, The present project intends to further define the expression pattern of PIK3CA, NF-κB and STAT3 in CD44+CD117+ in ovarian cancer cells in larger samples and a longer period, to explore the mechanism of activation for PIK3CA/NF-κB/STAT3 signaling and its role of regulation on chemotherapy sensitivity and the characteristics of stem cell in CD44+CD117+ ovarian cancer cells in vitro and in vivo, and to provide the noval theoretical and experimental basis for the prediction of response to postoperative chemotherapy and the individualized therapy in ovarian cancer patients .