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

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. Ci...
Source: Anti-Cancer Drugs - Category: Cancer & Oncology Tags: Original Studies Source Type: research