Basic research of cancer stem cell for therapeutic target in cisplatin-resistant ovarian cancer.

上皮间质转化（EMT）是肿瘤侵袭、转移和耐药的重要环节。我们研究了拓扑替康是否在体外和体内卵巢癌模型中增加顺铂的疗效。拓扑替康可抑制顺铂诱导的卵巢癌耐药细胞Akt活化，并调节EMT相关因子。此外，G蛋白偶联受体30是一种7-跨膜雌激素受体，与传统的雌激素受体一起发挥作用，以调节细胞对雌激素的反应。我们的研究表明GPR 30表达与EMT表型、侵袭性增殖和多药耐药有关。免疫组化结果显示，GPR 30和EGFR的表达降低了上皮性卵巢癌的生存率。

Epithelial-mesenchymal-transition(EMT) is recently identified as a important step in the invasion, metastasis, and chemo-resistance of cancer. We investigated whether topotecan increase the efficacy of cisplatin in in vitro and in vivo ovarian cancer models. Topotecan significantly inhibited the cisplatin-induced Akt activation, and regulated EMT-related factors in cisplatin-resistant ovarian cancer cell line. Furthermore, G protein-coupled receptor 30 is a 7-transmembrane estrogen receptor that functions alongside traditional estrogen receptors to regulate cellular responses to estrogen. In our studies suggested that GPR30 expression is linked to EMT phenotype, aggressive proliferation, and multiple drug resistance. Immunohistochemical examination revealed that expression of both GPR30 and EGFR contributes lower survival rates in epithelial ovarian cancer.