Long non‑coding RNA AK001796 contributes to cisplatin resistance of non‑small cell lung cancer.

Cisplatin (DDP)-based chemotherapy is the most widely used therapy for non-small cell lung cancer (NSCLC). However, the existence of chemoresistance has become a major limitation in its efficacy. Long non-coding RNAs (lncRNAs) have been shown to be involved in chemotherapy drug resistance. The aim of the present study was to investigate the biological role of lncRNA AK001796 in cisplatin-resistant NSCLC A549/DDP cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis was performed to monitor the differences in the expression of AK001796 in cisplatin-resistant (A549/DDP) cells and parental A549 cells. Cellular sensitivity to cisplatin and cell viability were examined using an MTT assay. Cell apoptosis and cell cycle distribution were measured using flow cytometry. The expression levels of cell cycle proteins cyclin C (CCNC), baculoviral IAP repeat containing 5 (BIRC5), cyclin-dependent kinase 1 (CDK1) and G2 and S phase-expressed 1 (GTSE1) were assessed using RT-qPCR and western blot analyses. It was found that the expression of AK001796 was increased in A549/DDP cells, compared with that in A549 cells. The knockdown of AK001796 by small interfering RNA reduced cellular cisplatin resistance and cell viability, and resulted in cell-cycle arrest, with a marked increase in the proportion of A549/DDP cells in the G0/G1 phase. By contrast, the knockdown of AK001796 increased the number of apoptotic cancer cells during cisplatin treatment. It was also shown that the knockdown of AK001796 positively induced the expression of cell apoptosis-associated factors, CCNC and BIRC5, and suppressed the expression of cell cycle-associated factors, CDK1 and GTSE5. Taken together, these findings indicated that lncRNA AK001796 increased the resistance of NSCLC cells to cisplatin through regulating cell apoptosis and cell proliferation, and thus provides an attractive therapeutic target for NSCLC.