N6-methyladenosine modification of hypoxia-inducible factor-1α regulates Helicobacter pylori-associated gastric cancer via the PI3K/AKT pathway

Figure 2 Hypoxia-inducible factor-1α overexpression promotes the activation of PI3K/AKT pathway and the malignant behaviors of cells. A: Quantitative reverse transcription-polymerase chain reaction showed that hypoxia-inducible factor-1α (HIF-1α) plasmid was successfully transfected into gastric epithelial cells; B and C: Protein levels were analyzed by Western blot, including HIF-1α, p-PI3K, PI3K, p-AKT, AKT, N-cadherin, Vimentin, ZEB1, MMP2, and MMP9, all normalized to β-actin. These proteins respectively represented the PI3K/AKT pathway, epithelial-mesenchymal transition, and cell invasion ability; D: Cell counting kit-8 assay was utilized to evaluate cell viability; E and F: Wound healing assay was conducted to test the migration ability. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001, compared with pcDNA3 or Hp27 + pcDNA3 group. Hp27: H. pylori 27 strain; HIF-1α: Hypoxia-inducible factor-1α.