目的 分析miR-130a在上皮性卵巢癌铂类敏感与耐药患者血清中的表达情况，探讨其耐药的相关机制。方法 选取32例上皮性卵巢癌铂类化疗耐药患者及30例化疗敏感患者，采用实时荧光定量PCR检测受试者血清中miR-130a表达差异，ELISA法检测血清中人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(phosphatase and tensin homolog deleted on chromosome ten，PTEN)、B淋巴细胞瘤-2基因（B-cell lymphoma-2，BCL-2）表达情况。结果 耐药组患者血清miR-130a和BCL-2表达均高于敏感组，而PTEN表达低于敏感组（P均＜0.05）。且随着组织学分级增加及淋巴转移的发生，耐药组患者血清miR-130a表达量显著升高（P<0.05）。结论 MiR-130a可能通过抑制PTEN激活PI3K/AKT信号通路、上调BCL-2抑制肿瘤细胞凋亡参与上皮性卵巢癌铂类化疗耐药的产生，miR-130a有望成为逆转上皮性卵巢癌化疗耐药的基因治疗新靶点。
英文摘要:
Objective To determine the expression of miR-130a in patients with epithelial ovarian cancer and its association with platinum resistance. Methods 32 patients with platinum resistance and 30 patients without platinum resistance were recruited in this study. Real-time PCR was performed to detect the expression of miR-130a in the serum samples of the patients. ELISA was used to measure the expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and B-cell lymphoma-2 (BCL-2). Results Platinum-resistant patients had significantly higher levels of expression of miR-130a and BCL-2, and lower level of PTEN than platinum-sensitive patients （P<0.05）. The expression level of miR-130a increased with increased severity in histological classification and appearance of lymph node metastasis in the platinum-resistant patients (P<0.05).Conclusion MiR-130a may mediate the generation of platinum resistance in epithelial ovarian cancer through inhibiting PTEN to activate PI3K/AKT signaling pathway and increasing BCL-2 to inhibit tumor cell apoptosis. MiR-130a may be a new potential target of gene therapy in platinum-resistant ovarian cancers.
