Long noncoding RNA Linc00210 promotes non-small cell lung cancer progression via sponging miR-16-5p/PTK2 axis

OBJECTIVE: Long noncoding RNAs (lncRNAs) are important regulators involved in a variety of cancer development. However, the role of Linc00210 in non-small cell lung cancer (NSCLC) remains unknown. This study aims to investigate the clinical value of Linc00210 in NSCLC patients and the biological functions of Linc00210 in NSCLC. PATIENTS AND METHODS: Gene expression in NSCLC tissues and cell lines was detected using qRT-PCR or Western blot. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and colony formation assays were conducted to evaluate the effect of Linc00210 on NSCLC cell proliferation. Transwell assay and annexin V-Fluorescein 5-isothiocyanate (FITC)/Propidium Iodide (PI) were done to analyze the effect of Linc00210 on cancer cell invasion and apoptosis, respectively. Luciferase reporter assay and RIP assay were performed to determine the target of Linc00210 and miR-16-5p. Besides, these assays were used to determine reciprocally inhibition of each other-controlled NSCLC cell behaviors. In vivo tumorigenesis experiments were applied to exhibit subcutaneous tumor growth. RESULTS: Linc0021 was highly expressed in NSCLC tissues and cell lines. Knockdown of Linc00210 inhibited cancer cell proliferation and invasion, and increased cell apoptosis, and regulated the expression of Cyclin A1, proliferating cell nuclear antigen (PCNA), E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Further data showed Linc00210 bound to and directly modulated the miR-16-5p levels. Impressively, overexpression of miR-16-5p suppressed NSCLC cell proliferation and invasion, but increased cell apoptosis, and these behaviors could be overturned by overexpression of Linc00210 in vitro and in vivo. Finally, Linc00210 and miR-16-5p cooperatively controlled expression of protein tyrosine kinase 2 (PTK2), a miR-16-5p target. CONCLUSIONS: Linc00210/miR-16-5p/PTK2 signaling suggests a promising novel strategy for anti-NSCLC therapy.