S100A6/miR193a regulates the proliferation, invasion, migration and angiogenesis of lung cancer cells through the P53 acetylation.

Non-small cell lung cancer (NSCLC) is accounted for 80% to 85% of the total lung cancer cases and still a difficult problem to solve at present. The present study was aimed to explore the effect of S100A6 on the proliferation, invasion, migration and angiogenesis in lung cancer cell lines with the change of miR-193a expression and P53 acetylation. The expression of S100A6, CDK2, cyclinD1, VEGF, ANGII, anti-acetylp53 (K373), K-AC, P21 and Noxa were analyzed by western blot analysis. RT-qPCR analysis was used to confirm the transfection effects. CCK-8 assay and flow cytometry were reflecting the cell proliferation. Wound healing assay and transwell assay were evaluating the cell invasion and migration. The dual-luciferase reporter assay was to confirm the S100A6 as a target of miR-193a. Immunofluorescence and immunohistochemical analysis were analyzing the S100A6 expression in cells and tumor tissues, respectively. As a result, S100A6 expression was increased in lung cancer cell lines and S100A6 expressed the highest in A549 cells which was chosen for the subsequent experiment. S100A6 overexpression promoted the proliferation, invasion, migration and angiogenesis of lung cancer cells with the promotion of degradation of P53 acetylation. In addition, S100A6 was demonstrated to be a target of miR193a. Moreover, miR193a expression was decreased in lung cancer cell lines and miR193a expressed the lowest in A549 cells which was chosen for the subsequent experiment. And, miR193a overexpression inhibited the proliferation, invasion, migration and angiogenesis of lung cancer cells with the enhancement of P53 acetylation. The effects of S100A6 overexpression and miR193a overexpression on tumor growth in vivo experiments were the same with that in the cell experiments. In conclusion, this study indicated that S100A6 overexpression could promote the proliferation, invasion, migration and angiogenesis of lung cancer cells by inhibiting the P53 acetylation and miR193a overexpression could reversed the above effects by decreasing the S100A6 expression in both vitro and vivo experiments.