MiR-1269a acts as an onco-miRNA in non-small cell lung cancer via down-regulating SOX6

• Published in: European review for medical and pharmacological sciences Vol. 22; no. 15; p. 4888
• Main Authors: Jin, R-H, Yu, D-J, Zhong, M
• Format: Journal Article
• Language: English
• Published: Italy 01.08.2018
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_201808_15625

Lung cancer, especially non-small cell lung cancer (NSCLC), remains one of the leading death-causing malignant tumors worldwide. MicroRNAs (miRNAs) have been identified to participate in the development and progression of NSCLC. However, the role of miR-1269a in NSCLC still needs to be elucidated. The objective of this study was to investigate the function of miR-1269a in NSCLC and its underlying mechanism. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was utilized to measure the expression level of miR-1269a in NSCLC tissues and cell lines. After transfection with miR-1269a mimics or inhibitors, the expression level of miR-1269a in NSCLC was up- or down-regulated. Cell Counting Kit-8 (CCK-8) assay and colony formation assay were used to measure cell proliferation ability. Flow cytometry assay was applied to verify the cell cycle distributions of established cell lines. The potential target of miR-1269a was determined by using dual-luciferase and Western blot assays. miR-1269a was significantly over-expressed in NSCLC tissues than that in adjacent normal tissues. The expression of miR-1269a was also up-regulated in NSCLC-derived cell lines. Up-regulation of miR-1269a improved the abilities of cell proliferation, colony formation, and induced cell cycle transition. Meanwhile, down-regulation of miR-1269a decreased the capacities of cell proliferation, colony formation, and arrested the cell cycle. It was further implicated that SOX6 was verified as a target of miR-1269a in NSCLC and over-expressed SOX6 could rescue the effect of miR-1269a up-regulation. Our study demonstrated that miR-1299a could function as an onco-miRNA in NSCLC and promote NSCLC growth via down-regulating the expression of SOX6.