Autor: |
Linrong Pang, Jinger Lu, Jia Huang, Caihong Xu, Hui Li, Guangbo Yuan, Xiaochun Cheng, Jun Chen |
Předmět: |
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Zdroj: |
Oncology Letters; Dec2017, Vol. 14 Issue 6, p7745-7752, 8p, 1 Chart, 7 Graphs |
Abstrakt: |
The aim of the present study was to investigate the effects of microRNA (miR‑)146a on the cisplatin sensitivity of the non‑small cell lung cancer (NSCLC) A549 cell line and study the underlying molecular mechanism. The differences in expression of miRNAs between A549 and A549/cisplatin (A549/DDP) cells were determined, and miR‑146a was selected to study its effect on cisplatin sensitivity of A549/DDP cells. miR‑146a mimic and inhibitor transient transfection systems were constructed using vectors, and A549/DDP cells were infected with miR‑146a mimic and inhibitor to investigate growth, apoptosis and migration. The directed target of miR‑146a was determined and the underlying molecular mechanism was validated in the present study. The results of the present study demonstrated that miR‑146a was down-regulated in NSCLC A549/DDP cells, compared with A549 cells. The overexpression of miR‑146a induced apoptosis and inhibited the growth and invasion of A549/DDP cells, which resulted in increased cisplatin sensitivity in NSCLC cells. The JNK2 gene was determined as the direct target of miR‑146a, and may be activated by the overexpression of miR‑146a. Additionally, JNK2 activated the expression of p53 and inhibited B cell lymphoma 2. The upregulation of miR‑146a increased cisplatin sensitivity of the A549 cell line by targeting JNK2, which may provide a novel method for treating NSCLC cisplatin resistance. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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