LncRNA BLACAT1 is involved in chemoresistance of non-small cell lung cancer cells by regulating autophagy

The aim of the present study was to determine the effect of the long non-coding RNA (lncRNA) bladder cancer-associated transcript 1 (BLACAT1) in chemoresistance of non-small cell lung cancer (NSCLC) cells. Expression of lncRNA BLACAT1, microRNA (miR)-17, autophagy-related protein 7 (ATG7), multidrug-resistance protein 1 (MRP1), and the autophagy-associated proteins light chain 3 (LC3)-II/LC3-I and Beclin 1 were detected using the reverse transcription-quantitative polymerase chain reaction and western blot analysis. Cell viability was determined using an MTT assay. The interaction between BLACAT1 and miR-17 was determined using RNA immunoprecipitation and RNA pull-down assays. A cisplatin (DDP)-resistant NSCLC cell A549/DDP xenograft model in nude mice was established to investigate the effect of BLACAT1 on the chemoresistance of NSCLC cells. Compared with in DDP-sensitive NSCLC cells, expression of BLACAT1, ATG7, MRP1, LC3-II/LC3-I and Beclin 1 was significantly upregulated in DDP-resistant NSCLC cells, whereas miR-17 was downregulated in DDP-resistant NSCLC cells. Short interfering RNA against BLACAT1 decreased the viability of DDP-resistant NSCLC cells. In addition, BLACAT1 interacted with miR-17, and negatively regulated miR-17. BLACAT1 promoted ATG7 expression through miR-17, and facilitated autophagy and promoted chemoresistance of NSCLC cells through miR-17/ATG7. Finally, in vivo experiments indicated that inhibition of BLACAT1 ameliorated the chemoresistance of NSCLC. BLACAT1 was upregulated in DDP-resistant NSCLC cells, and promoted autophagy and chemoresistance of NSCLC cells through the miR-17/ATG7 signaling pathway.