微小RNA-107通过靶向非小细胞肺癌中的抗凋亡因子Bcl-w增强对紫杉醇的化疗敏感性。
MiRNA-107 enhances chemosensitivity to paclitaxel by targeting antiapoptotic factor Bcl-w in non small cell lung cancer.
作者信息
Lu Chaojing, Xie Zhibing, Peng Qingzhen
机构信息
Department of Thoracic Surgery, Changhai HospitalShanghai, China.
Department of Respiratory Medicine, Xiaogan Central Hospital, Wuhan University of Science and TechnologyXiaogan, China.
出版信息
Am J Cancer Res. 2017 Sep 1;7(9):1863-1873. eCollection 2017.
The aim of this study is to elucidate whether and how miR-107 participates in the modulation of paclitaxel sensitivity in non small cell lung cancer (NSCLC). By qRT-PCR, we found that miR-107 is significantly down-regulated in paclitaxel-resistant A549/Taxol cells compared with corresponding paclitaxel-sensitive counterparts. Overexpression of miR-107 suppresses paclitaxel resistance of A549/Taxol cells through directly inhibiting Bcl-w. Overexpression of miR-107 promotes apoptosis and inhibits proliferation and mobility of A549/Taxol cells under treatment with paclitaxel . Moreover, miR-107 inhibits paclitaxel resistance in xenograft model. MiR-107/Bcl-w axis regulates paclitaxel chemoresistance through PI3K-Akt pathway. Our results suggest that up-regulation of miR-107 resensitizes paclitaxel-resistant NSCLC cells by targeting Bcl-w, which reveals a potential mechanism of miR-107 in reversing drug resistance.
本研究旨在阐明miR-107是否以及如何参与非小细胞肺癌（NSCLC）中紫杉醇敏感性的调节。通过qRT-PCR，我们发现与相应的紫杉醇敏感细胞相比，miR-107在紫杉醇耐药的A549/Taxol细胞中显著下调。miR-107的过表达通过直接抑制Bcl-w来抑制A549/Taxol细胞的紫杉醇耐药性。miR-107的过表达促进了紫杉醇处理下A549/Taxol细胞的凋亡，抑制了其增殖和迁移。此外，miR-107在异种移植模型中抑制紫杉醇耐药性。miR-107/Bcl-w轴通过PI3K-Akt途径调节紫杉醇化疗耐药性。我们的结果表明，miR-107的上调通过靶向Bcl-w使紫杉醇耐药的NSCLC细胞重新敏感，这揭示了miR-107在逆转耐药性中的潜在机制。
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