Lung cancer A549 cells suppressed with overexpressed HNF1B or PCDHA13 inhibited PI3K/AKT phosphorylation

BACKGROUND: Lung cancer is the most revenant and deadly tumors around the world. Here we aimed to explore the effects of hepatocyte nuclear factor 1B (HNF1B) and PCDHA13 overexpression on PI3K/AKT phosphorylation and malignant biological behavior in lung cancer A549 cells. METHODS: HNF1B and PCDHA13 were amplified, and their overexpression plasmids were constructed for transfection. RT-PCR was used to detect the mRNA levels of HNF1B and PCDHA13. Cell proliferation and cell apoptosis were detected by clone formation experiments and flow cytometry, respectively, while cell invasion was studied by Transwell assay. The expression of survivin, PCNA, Caspase-3, Caspase-9, VEGF, and fibronectin was detected using immunoblotting, as was PI3K/AKT phosphorylation. RESULTS: The level of HNF1B mRNA expression was significantly higher in the pcNDA-HNF1B group than in the control group (P<0.05), and the level of PCDHA13 mRNA expression in the pcNDA-PCDHA13 group was also significantly increased (P<0.05). The clone formation rate and cell invasion count in pcNDA-HNF1B or pcNDA-PCDHA13 transfected groups were significantly reduced in comparison with the control group, which were further validated with the protein expression levels of survivin, PCNA, VEGF, and fibronectin (P<0.05). However, the apoptosis rate, and the cleaved caspase3/caspase3 and cleaved caspase9/caspase9 protein expression ratios were all significantly increased (P<0.05). Cells transfected with pcNDA-HNF1B or pcNDA-PCDHA13 showed decreased levels of PI3K/AKT phosphorylation (P<0.05). CONCLUSIONS: Overexpression of HNF1B and PCDHA13 inhibits the phosphorylation of PI3K/AKT and hinders the malignant biological behavior of lung cancer A549 cells.