Abstract. 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)

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 elucida‐ tion. In the present study, LINC00707 and microRNA (miR)‐145 expression levels were measured using reverse transcription‐quan‐ titative 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. Introduction Non‐small‐cell lung cancer (NSCLC) accounts for ~85% of all lung cancer cases, demonstrating a high degree of mortality and poor survival worldwide (1). In recent years, substantial advances have been achieved in NSCLC diagnosis and treat‐ ment; however, the 5‐year survival rate has remained unchanged at 15% (2). Cisplatin (DDP) is a first‐line drug used in NSCLC chemotherapy; however, resistance to chemotherapy drugs administered after surgeries limits the prognosis of patients, as well as the use of DDP in clinical applications (3). Therefore, the molecular mechanisms underlying DDP resistance need to be urgently elucidated in order to improve the survival rate of patients with NSCLC. Long non‐coding RNAs (lncRNAs) are non‐protein coding RNAs that are greater than 200 nucleotides in length (3). Numerous studies have indicated that lncRNAs are capable of regulating gene expression at the transcrip‐ tional, post‐transcriptional and epigenetic levels, and serve an important role in human cancer development, prognosis and drug resistance (4,5). Recent studies have associated certain lncRNAs, including CCAT1 (6) and TRPM2‐AS (7), with DDP resistance in lung cancer. Long intergenic non‐coding RNA 00707 (LINC00707), located on chromosome 10p14, has also been associated with the development and progres‐ sion of cancers, including hepatocellular carcinoma (8), gastric cancer (9) and lung cancer (10). However, the function and underlying mechanism of LINC00707 in the progression of DDP resistance in NSCLC remains largely unclear. Recently, emerging evidence has revealed that lncRNAs are able to serve as competing endogenous RNAs or microRNA (miRNA/miR) sponges, and induce regulatory effects on miRNAs and miRNA‐targeted mRNAs (11). miRNAs are a group of evolutionarily conserved, single‐stranded, non‐coding RNAs (21‐25 nucleotides in length) that regu‐ late post‐transcriptional gene expression by targeting the 3'‐untranslated regions (3'‐UTRs) of their target mRNAs (12). Aberrant expression of various miRNAs has been suggested to contribute to DDP resistance in human cancers (13). miR‐145, a tumor suppressor miRNA, has been reported to be down‐ regulated in several types of human cancers, including lung cancer (14). Furthermore, Zhan et al (15) reported that miR‐145 promoted multidrug resistance protein 1 (MRP1) mRNA degradation and, therefore, sensitized gallbladder cancer cells Silencing long intergenic non‐coding RNA 00707 enhances cisplatin sensitivity in cisplatin‐resistant non‐small‐cell lung cancer cells by sponging miR‐145 HONGDE ZHANG, YI LUO, WENLI XU, KANG LI and CHANGZHENG LIAO Central Laboratory, Longgang District Central Hospital of Shenzhen, Shenzhen, Guangdong 518116, P.R. China Received April 23, 2019; Accepted September 2, 2019 DOI: 10.3892/ol.2019. 10959 Correspondence to: Dr Hongde Zhang, Central Laboratory, Longgang District Central Hospital of Shenzhen, 1228 Shenhui Road, Longgang, Shenzhen, Guangdong 518116, P.R. China E‐mail: labzhd@126.com