卵巢癌对顺铂和紫杉醇耐药的分子机制

卵巢癌致死率居女性生殖道恶性肿瘤之首，严重威胁女性的生命健康。肿瘤细胞减灭术及铂类联合紫杉醇的系统化疗是治疗卵巢癌的金标准。因卵巢癌起病隐匿，多数卵巢癌患者确诊时已属晚期，而晚期肿瘤易对目前的化疗药物产生抗药性，因此化疗耐药已成为提高卵巢癌治愈率的关键制约因素。明确化疗耐药的分子机制对探索有效的靶向治疗、研发逆转耐药的新药物具有极其重要的价值，从而提高化疗敏感性和逆转化疗耐药。卵巢癌化疗耐药的形成是多基因、多因素、多水平共同参与的结果，主要的分子机制有抗凋亡、促生存、细胞内药物排出增多、细胞解毒及DNA修复功能增强等。卵巢癌对顺铂和紫杉醇耐药的分子机制尚无定论，现就其可能的耐药机制进行综述。

Molecular Mechanisms of Cisplatin and Paclitaxel Resistance for Ovarian Cancer

Ovarian cancer is the most lethal in female reproductive carcinomas, seriously threatening the lives and health of female. Cytoreductive surgery and platinum-based cytotoxic chemotherapy are standard therapies for the treatment of ovarian cancer. The majority of ovarian cancer patients are diagnosed at advanced stages due to insidious onset, while advanced ovarian cancer patients tend to become refractory to current chemotherapeutic agents. Therefore, a critical contributor to the poor survival rate is the development of chemoresistance. There is particularly significant implication to elucidate the molecular mechanisms of chemoresistance for exploring efficient targeted therapies and developing novel therapeutic agents that can improve chemotherapy sensitivity and reverse chemoresistance. The development of chemoresistance for ovarian cancer is the results of polygenic and multifactorial interactions at different levels, the significant mechanisms involve in anti-apoptosis, pro-survival, drug efflux, detoxification, DNA repair and so on. The molecular mechanisms of ovarian cancer resistance for cisplatin and paclitaxel are uncertain, now this report aims to review the possible mechanisms.