Fig. 3: FBXO22 promotes tumor angiogenesis and metastasis by upregulating HIF-1α and VEGF-A through the PI3K/AKT signaling pathway.
From: FBXO22 promotes HCC angiogenesis and metastasis via RPS5/AKT/HIF-1α/VEGF-A signaling axis
A The heatmap shows the difference between HLF cell control and shFBXO22 expression. B The KEGG analysis of DEGs is displayed. The PI3K-AKT signaling pathway is marked in red. C Overexpression and knockdown of FBXO22 in Hep3B and MHCC97H cells resulted in changes in AKT phosphorylation. D Alterations in the levels of RPS5, AKT, and P-AKT (S473) proteins were observed in both the cytoplasm and nucleus following FBXO22 knockdown. E Treatment with the AKT specific inhibitor (LY294002) (20 μM) reversed the change of HIF-1α and VEGF-A expression, as well as AKT phosphorylation, induced by overexpression and knockdown of FBXO22 in Hep3B cells. LY294002 was administered 24 h after transfection. F, G LY294002 has the ability to inhibit the overexpression of FBXO22, thereby preventing tubular formation and migration and invasion of HUVECs. H LY294002 can prevent the migration and invasion of FBXO22 overexpressed Hep3B cells. Data and error bars are presented as mean ± SD from triplicate independent replicate experiments. The data were analyzed using a paired Student’s t-test for experiments (F–H). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
