Silencing long intergenic non-coding RNA 00707 enhances cisplatin sensitivity in cisplatin-resistant non-small-cell lung cancer cells by sponging miR-145.

The aberrant expression of long non-coding RNAs is closely associated with drug resistance in multiple types of cancer. Long intergenic non-coding RNA 00707 (LINC00707) has previously been reported to be an oncogene able to promote lung adenocarcinoma cell proliferation and metastasis. However, its role in the progression of cisplatin (DDP) resistance in non-small-cell lung cancer (NSCLC) requires further elucidation. In the present study, LINC00707 and microRNA (miR)-145 expression levels were measured using reverse transcription-quantitative PCR (RT-qPCR). MTT and flow cytometric assays were performed to evaluate the IC50 value of DDP and cell apoptosis, respectively. Bcl-2, Bax, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-gp) mRNA and protein expression were detected using RT-qPCR and western blotting, respectively. The interaction between LINC00707 and miR-145 was explored using a luciferase reporter assay. LINC00707 expression was found to be significantly upregulated in DDP-resistant A549 cells (A549/DDP) cells when compared with that in parental A549 cells. LINC00707 knockdown reduced the IC50 value of DDP, enhanced apoptosis and inhibited Bcl-2, MRP1 and P-gp expression, while promoting Bax expression in A549/DDP cells. miR-145 expression was found to be significantly decreased in A549/DDP cells when compared with in A549 cells. LINC00707 directly interacted with miR-145 and negatively regulated its expression. Furthermore, miR-145 downregulation weakened the effect of LINC00707 knockdown in A549/DDP cells. Therefore, silencing of LINC00707 enhanced DDP sensitivity in A549/DDP cells by sponging miR-145, thereby shedding light on LINC00707 and its corresponding molecular mechanisms involved in the progression of DDP resistance in NSCLC cells.