Circ_0001058 represses the progression of lung adenocarcinoma through governing of the miR-486-5p/TEK signaling axis.

The most common type of lung cancer is lung adenocarcinoma. Emerging views believe that circular RNA (circRNA) participates in its pathogenesis. The objective of this study is to find out the potential functions and mechanisms of circ_0001058 in lung adenocarcinoma pathogenesis. To detect circ_0001058, miR-486-5p and TEK tyrosine kinase (TEK) receptor tyrosine kinase expressions, real-time quantitative PCR (RT-qPCR) and western blotting were performed. Cell functions, including proliferation, apoptosis and invasion, were then evaluated using cell counting kit-8, caspase-3 activity and transwell assays, respectively. To establish the role of circ_0001058 in tumorigenesis, nude mice were utilized as in-vivo models. The predicted binding relationships of miR-486-5p to circ_0001058 or TEK were further verified by performing a dual-luciferase assay and ribonucleoprotein immunoprecipitation (RIP) analysis. Decreased circ_0001058 expression was observed in lung adenocarcinoma cells and tissue specimens. Circ_0001058 was predominantly situated in the cytoplasm and was greatly resistant to RNase R digestion. Circ_0001058 overexpression restrained A549 and PC9 cells' abilities to proliferate, survive and invade, and it also repressed tumorigenesis in the animal models. Circ_0001058 directly targeted miR-486-5p and depleted its expression. Restoring miR-486-5p could invert the inhibitory effects of circ_0001058 in the cancer cell phenotypes. Furthermore, miR-486-5p targeted TEK, so the inhibitory effects of TEK overexpression on the malignant behaviors of A549 and PC9 cells could also be abolished by miR-486-5p restoration. Circ_0001058 overexpression blocked the malignant development of lung adenocarcinoma via modulation of the miR-486-5p/TEK pathway. These results contribute new insights on the pathogenesis of lung adenocarcinoma.