马拉特1
顺铂
A549电池
肺癌
下调和上调
活力测定
癌症研究
细胞凋亡
细胞培养
免疫印迹
细胞
生物
化学
医学
肿瘤科
化疗
基因
生物化学
长非编码RNA
遗传学
作者
Zhixian Fang,Wenyu Chen,Zuguo Yuan,Xing’e Liu,Hao Jiang
标识
DOI:10.1016/j.biopha.2018.02.130
摘要
Multiple drug resistance is the main reason for chemotherapeutic failure in lung cancer patients with complex molecular mechanisms. LncRNA-MALAT1 plays functional roles in the progression of carcinomas and development of drug resistance. We aimed to identify the role of MALAT1 in DDP-resistant non-small cell lung cancer as well as potential mechanisms. Human lung cancer cell line A549 and the DDP-resistant cell line A549/DDP were used. Cell transfection was performed to establish A549/MALAT1 and A549/DDP/shMALAT1 cells. The qRT-PCR analysis was performed to detect lncRNA-MALAT1 level. Cell viability, colony formation assay, apoptosis analysis, western blot analysis, immunohistochemistry, and animal study were carried out. MALAT1 was upregulated in DDP-resistant A549 cell line. MALAT1 decreased DDP sensitivity in vitro and in vivo by upregulating MRP1 and MDR1 via STAT3 activation. Overexpression of MALAT1 contributed to the DDP resistance and might confer a potently poor prognosis.
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