文章摘要
赵洁婷,钟文,徐建平.microRNA-21促进人肺腺癌细胞A549对顺铂耐药性的研究[J].安徽医药,2017,21(6):1082-1086.
microRNA-21促进人肺腺癌细胞A549对顺铂耐药性的研究
microRNA-21 induces drug resistance to cisplatin in human lung cell line A549
投稿时间:2016-08-19  
DOI:
中文关键词: 肺癌  microRNA-21  耐药  PI3K/AKT
英文关键词: 
基金项目:安徽省自然科学基金项目(1608085QH217)
作者单位E-mail
赵洁婷 安徽省胸科医院病理科,安徽 合肥 230022  
钟文 安徽省立医院病理科,安徽 合肥 230001  
徐建平 安徽省胸科医院病理科,安徽 合肥 230022 xjpxkbl@163.com 
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中文摘要:
      目的 研究microRNA-21(miR-21)对人肺腺癌细胞A549对于顺铂耐药性的影响及分子机制。方法 MTT法检测A549和顺铂耐药株A549/CDDP对于顺铂的敏感性,以及在A549细胞中过表达miR-21和在A549/CDDP细胞中抑制miR-21表达后对顺铂敏感性的影响;RT-PCR方法检测A549和A549/CDDP中miR-21表达情况;Western blotting检测PI3K/AKT,核因子-κB(NF-κB)信号通路的激活情况以及在过表达miR-21和抑制miR-21表达后细胞中AKT信号通路的活性变化情况。结果 相对于A549细胞,A549/CDDP对顺铂的敏感性有明显降低,而细胞中miR-21表达则明显增多。Western blotting结果表明:与A549细胞相比,A549/CDDP细胞PI3K/AKT通路被激活,NF-κB通路没有明显变化。过表达miR-21可以激活PI3K/AKT信号通路并提高A549细胞对顺铂的耐药性,相反地,抑制miR-21表达抑制了A549/CDDP细胞中的AKT通路的活化情况并降低了A549/CDDP细胞对顺铂的耐药性。结论 miR-21可以促进肺癌细胞A549对顺铂的耐药性,其机制与PI3K/AKT信号通路的激活有关。
英文摘要:
      Objective To investigate the molecular mechanism of microRNA-21 (miR-21) induced-drug resistance in human lung cell line A549 cells.Methods The sensibility of A549 cells and A549/CDDP cells to cisplatin and the effect of miR-21 on sensibility of A549 cells or A549/CDDP cells to cisplatin was measured by MTT assay.The expression of miR-21 in A549 cells and A549/CDDP cells was detected by RT-PCR.Western blotting was used to detect the activation of AKT and NF-κB signaling pathways.Results Compared to A549 cells,the resistance of A549/CDDP cells to cisplatin was significantly enhanced and the expression of miR-21 in A549/CDDP cells was also increased.The results of western blotting demonstrated that AKT signaling pathway,not NF-κB signaling pathway was activated.MiR-21 overexpression decreased the sensibility of A549 cells to cisplatin and activated AKT signaling pathway.Conversely,inhibition of miR-21 expression increased the sensibility of A549/CDDP cell to cisplatin and suppressed the activity of AKT signaling pathway.Conclusions miR-21 can induce drug resistance of human lung cell line A549 to cisplatin and molecular mechanism involve in activation of PI3K/AKT signaling pathway.
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