ArticleBMC cancer2026
AMPK/p38 MAPK signaling selectively enhances HIF-induced VEGF-A165 expression under hypoxic and low-glucose conditions in HepG2 cells to promote endothelial cell proliferation and migration.
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAngiogenesis is essential for tumor development and growth. Vascular endothelial growth factor-A (VEGF-A), a key regulator of angiogenesis, has several isoforms; however, their expression patterns and mechanisms of action are not fully understood. In this study, we aimed to investigate the expression patterns of VEGF-A isoforms and their effects on endothelial cell responses related to angiogenesis under hypoxic and low-glucose conditions, which are major features of the tumor microenvironment, using a hepatocellular carcinoma cell line (HepG2).
methodsWe cultured human liver cancer-derived cell lines under hypoxic and low-glucose conditions and analyzed the expression patterns of VEGF-A isoforms using an original enzyme-linked immunosorbent assay system that could separately detect human VEGF-A121 and VEGF-A165, which we had previously developed.
resultsThe addition of low-glucose conditions to a hypoxic environment increased VEGF-A mRNA and protein expression in HepG2 cells, particularly that of VEGF-A165. Since it is known that AMP-activated protein kinase (AMPK)/p38 mitogen-activated protein kinase (p38 MAPK) signaling increases the stability of VEGF-A mRNA, we investigated the involvement of this signal and found that activation of AMPK increased VEGF-A165 protein expression, while inhibition of AMPK and p38 MAPK reduced VEGF-A165 protein expression. Furthermore, the effects of VEGF-A isoforms on human umbilical vein endothelial cells (HUVECs) were examined. VEGF-A165 activated phosphorylation signals in HUVECs and upregulated their proliferation and migration abilities compared to VEGF-A121.
conclusionsThese findings suggest that AMPK/p38 MAPK signaling selectively enhances hypoxia-inducible factor-induced VEGF-A165 expression in tumors and promotes endothelial cell proliferation and migration, which may contribute to angiogenesis in vivo.
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