| 王银华,谷 宏,周 勤.miR-21促进肺癌EGFR-TKI耐药细胞株上皮—间质细胞转化的研究[J].肿瘤学杂志,2014,20(8):654-658. |
| miR-21促进肺癌EGFR-TKI耐药细胞株上皮—间质细胞转化的研究 |
| MiR-21 Promotes Epithelial to Mesenchymal Transition in EGFR-TKI Resistant Lung Cancer Cells |
| 投稿时间：2014-05-23 |
| DOI：10.11735/j.issn.1671-170X.2014.08.B009 |
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| 中文关键词: 肺肿瘤 获得性耐药 miR-21 EMT |
| 英文关键词:lung neoplasms acquired resistance miR-21 EMT |
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| 中文摘要: |
| 摘 要：［目的］ 研究miR-21是否可以调控上皮—间质转化（EMT）而参与肺癌获得性耐药。［方法］ 使用HCC827细胞（EGFR基因19外显子缺少的肺腺癌细胞株），在此细胞的基础上培养吉非替尼耐药细胞株HCC827/GR。检测耐药细胞株中miR-21的表达，同时观察耐药细胞的形态变化，及在耐药细胞株中抑制miR-21表达后检测耐药细胞株的侵袭能力及EMT相关蛋白E-cadherin和Vimentin的表达。［结果］ 与敏感细胞株HCC827相比，HCC827/GR细胞株对吉非替尼的耐药倍数约为100倍；同时在耐药细胞株中我们发现miR-21较敏感株表达增高约5.3倍，同时细胞形态发生了明显变化。通过检测EMT相关蛋白，我们发现耐药细胞株中间质相关蛋白Vimentin明显高表达，而上皮相关蛋白E-cadherin明显低表达，当miR-21被抑制后，耐药细胞株侵袭能力下降，同时Vimentin表达量下降，而E-cadherin表达量增高。［结论］ miR-21可能通过促进EMT参与肺癌EGFR-TKI的获得性耐药。 |
| 英文摘要: |
| Abstract：［Purpose］To investigate the association of epithelial mesenchymal transition and miR-21 in EGFR-TKI acquired resistant cell line—HCC827/GR.［Methods］ Resistant cell line HCC827/GR based on EGFR-TKI sensitive cell line HCC827 ( exon 19 deletion in EGFR gene) was established. The expression of miR-21 was detected by RT-PCR，meanwhile the morphological change was observed. MiR-21 was inhibited in HCC827/GR and invasion capacity and EMT related biomarkers such as E-cadherin and Vimentin were detected by Western blot. ［Results］ Compared with HCC827，HCC827/GR demonstrated 100 times resistance to EGFR-TKI. Moreover，we observed that miR-21 was more than 5 folds higher in HCC827/GR compared with HCC827，and HCC827/GR demonstrated mesenchymal phenotype. We also found that expression of Vimentin increased while expression of E-cadherin decreased compared with HCC827. When miR-21 was inhibited in HCC827/GR，expression of Vimentin decreased while expression of E-cadherin increased.［Conclusion］ MiR-21 may promote EMT in lung cancer，which contributes to EGFR-TKI acquired resistance. |
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