Upregulation of miR-202-3p reduces Icotinib resistance in lung carcinoma A549/Ico cells

Journal of RNA i and Gene Silencing

Hong Yang¹ 

关键词: Hong Yang;    Cui-Ying Zhang;    Icotinib resistance;    miR-202-3p;    Lung carcinoma;    A549/Ico cells;   

DOI  :  

学科分类：生物科学（综合）

来源: Library Publishing Media

【 摘 要 】

Icotinib exerts a good anti-tumor efficacy on non-small cell lung cancer (NSCLC), while Icotinib resistance has become an important limiting factor in the clinical application. Studies have certified that a great quantity of microRNAs are involved in the development of cancer. Here we found that miR-202-3p was observably down-regulated in A549/Ico cells, which is a kind of Icotinibresistant lung cancer cells. Transfection of A549/Ico cells with miR-202-3p reversed the Icotinib resistance and increased cell apoptosis. Subsequently, we examined the expression of ADP-Ribosylation Factor-like 5A (ARL5A), the functional target of miR-202-3p, as well as the multi-drug resistant (MDR) related genes glutathione s transferase π (GST-π), Multi Drug Resistance 1 (MDR1), multidrug resistance-associated protein 1 (MRP1) and breast cancer resistance protein (BCRP), which were down-regulated following the upregulation of miR-202-3p in A549/Ico cells. Our study demonstrated that miR-202-3p transfection reduced Icotinib resistance in human lung cancer A549/Ico cells by modulation of its downstream target ARL5A and MDR-related genes expression. These findings suggest that miR-202-3p may function as a novel therapeutic candidate in patients with MDR lung cancer.

【 授权许可】

Unknown