Circular RNA hsa_circ_0012673 facilitates lung cancer cell proliferation and invasion via miR-320a/LIMK18521 axis.

Abstract

Lung cancer is one of the most malignant tumors with high morbidity and mortality in the world. The incidence and mortality of lung cancer were increased per year in many countries over the past 50 years. The increasing studies had shown that circular RNA (circRNA) was involved in the progression of lung cancer. Therefore, it was significant to seek the molecular mechanism of circ_0012673 in lung cancer. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to estimate the expression levels of circ_0012673, miR-320a and LIM domain kinase 1 (LIMK1) in lung cancer tissues and cells. 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry and transwell assays were recruited to evaluate proliferation, apoptosis and mobility of lung cancer cells, respectively. The relative protein expression levels of Vimentin, N-cadherin, E-cadherin and LIMK1 were determined with Western blot assay. The relationships among circ_0012673, miR-320a and LIMK1 were analyzed by starBase database, dual-luciferase reporter assay, and Pearson's correlation. Circ_0012673 was overexpressed in lung cancer tissues and cell lines. Loss-of-functional experiment confirmed that knockdown of circ_0012673 constrained proliferation, motility and Epithelial-Mesenchymal Transition (EMT), but induced apoptosis by targeting miR-320a. Furthermore, LIMK1 was a target of miR-320a in lung cancer cells. Elevated LIMK1 could abolish the overexpression of miR-320a induced effects on lung cancer cells. Mechanistically, circ_0012673 contributed to lung cancer progression through mediating miR-320a /LIMK1 pathway. Circ_0012673 was a tumor-promoter in lung cancer via acting as competing endogenous RNA to regulate LIMK1 expression by binding miR-320a.