Chen Cen, Wang Hong-jing, Yang Ling-Yun, Jia Xi-biao, Xu Pan, Chen Jing, Liu Ya
Sichuan Da Xue Xue Bao Yi Xue Ban. 2016 Jan;47(1):60-3.
To determine the expression of miR-130a in patients with epithelial ovarian cancer and its association with platinum resistance.
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).
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).
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.
确定miR-130a在上皮性卵巢癌患者中的表达及其与铂耐药性的关联。
本研究招募了32例铂耐药患者和30例无铂耐药患者。采用实时定量聚合酶链反应(Real-time PCR)检测患者血清样本中miR-130a的表达。采用酶联免疫吸附测定法(ELISA)检测第10号染色体缺失的磷酸酶和张力蛋白同源物(PTEN)及B细胞淋巴瘤-2(BCL-2)的表达水平。
铂耐药患者的miR-130a和BCL-2表达水平显著高于铂敏感患者,而PTEN水平低于铂敏感患者(P<0.05)。铂耐药患者中,miR-130a的表达水平随着组织学分级的加重及淋巴结转移的出现而升高(P<0.05)。
MiR-130a可能通过抑制PTEN激活PI3K/AKT信号通路并增加BCL-2以抑制肿瘤细胞凋亡,从而介导上皮性卵巢癌铂耐药的产生。MiR-130a可能是铂耐药卵巢癌基因治疗的一个新的潜在靶点。