The malignant phenotype of gefitini-resistant non-small cell lung cancer mediated by miR-501 targeted BLID
GE Ling1 CHEN Hejian2 XU Hangdi3
1.Department of Pharmacy, Zhuji Hospital Affiliated to Wenzhou Medical University, Zhejiang Province, Zhuji 311800, China;
2.Department of Respiratory Medicine, Zhuji Hospital Affiliated to Wenzhou Medical University, Zhejiang Province, Zhuji 311800, China;
3.Medical College of Zhejiang University, Zhejiang Province, Hangzhou 310058, China
Abstract：Objective To explore the role of miR-501 in non-small cell lung cancer (NSCLC) with gefitinib resistance and its underlying mechanism. Methods The expression of miR-501 in NSCLC with gefitinib resistance serum and PC9/GR were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-501 on the malignant phenotype of PC9/GR was detected by CCK-8, scratch test and Transwell test. The online database was used to predict the potential target of miR-501 and to verify its specific role in PC9/GR. Results Compared with the healthy control people and the normal lung epithelial cell lines, the expression level of miR-501 in gefitini-resistant NSCLC patients serum and PC9/GR were increased, and the differences were highly statistically significant (P ＜ 0.01). Compared with the mimics NC, the proliferation, migration and invasion capacity of PC9/GR in the miR-501 mimics were increased, and the differences were highly statistically significant (P ＜ 0.01). The luciferase reporter assay confirmed that BLID was a direct target for miR-501. Compared with the miR-501 mimics+pcDNA3.1, the proliferation, migration and invasion of PC9/GR in the miR-501 mimics+ pcdna3.1-blid were decreased, and the differences were highly statistically significant (P ＜ 0.01). Conclusion The upregulation of miR-501 promoted the proliferation, migration, and invasion of geffitini-resistant NSCLC by inhibiting BLID. Therefore, miR-501 is a potential target for gefitinib-resistant NSCLC.
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2020, Vol. 17 
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