TEK Suppresses Lung Adenocarcinoma Cell Phenotypes by Interacting with miR-19a-3p

Background: We identified TEK as a key gene that that participates in lung adenocarcinoma cell migration and adhesion, and miR-19a-3p a potential upstream regulator of TEK. Both TEK and miR-19a-3p have been reported during lung cancer development. However, how TEK/miR-19a-3p interactome regulates lung adenocarcinoma remains unraveled. We herein aim to report a novel TEK/miR-19a-3p interactome in lung adenocarcinoma.Methods: The mRNA and protein expression of TEK in tissues and cell lines were determined using qPCR and Western blot, respectively. CCK-8 assay, EDU assay, flow-cytometry cell apoptosis assay, scratch assay, and cell-to-extracellular matrix adhesion assay were performed to detect the proliferation, apoptosis, migration, and adhesion of A549 and H1975 cell lines. Results：Both mRNA and protein levels of TEK were down-regulated in tumor tissues and cell lines. Compared with the control, the transfection of TEK overexpression plasmids into H1975 and A549 cells led to the significant inhibition of cancerous phenotypes. On the other hand, miR-19a-3p promoted lung adenocarcinoma cancerous cell phenotypes by downregulating TEK.Conclusions: TEK can be a potential LUAD tumor suppressor by interacting with miR-19a-3p. This novel interactome can be used as a novel therapy target for LUAD.