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Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes. | LitMetric

AI Article Synopsis

  • - Hypoxia plays a crucial role in cancer development, particularly in lung cancer, by influencing mechanisms that promote tumor progression and metastasis.
  • - It affects gene expression through hypoxia-inducible factors (HIFs), leading to processes like epithelial-to-mesenchymal transition (EMT) and angiogenesis, primarily via various signaling pathways.
  • - Additionally, hypoxia triggers metabolic changes, notably the Warburg effect, promoting a shift to glycolysis and increased GLUT1 expression, which supports cancer cell survival and growth.

Article Abstract

Hypoxia represents a frequent player in a number of malignancies, contributing to the development of the neoplastic disease. This review will discuss the means by which hypoxia powers the mechanisms behind cancer progression, with a majority of examples from lung cancer, the leading malignancy in terms of incidence and mortality rates (the frequent reference toward lung cancer is also for simplification purposes and follow up of the global mechanism in the context of a disease). The effects induced by low oxygen levels are orchestrated by hypoxia-inducible factors (HIFs) which regulate the expression of numerous genes involved in cancer progression. Hypoxia induces epithelial-to-mesenchymal transition (EMT) and metastasis through a complex machinery, by mediating various pathways such as TGF-β, PI3k/Akt, Wnt, and Jagged/Notch. Concomitantly, hypoxic environment has a vast implication in angiogenesis by stimulating vessel growth through the HIF-1α/VEGF axis. Low levels of oxygen can also promote the process through several other secondary factors, including ANGPT2, FGF, and HGF. Metabolic adaptations caused by hypoxia include the Warburg effect-a metabolic switch to glycolysis-and GLUT1 overexpression. The switch is achieved by directly increasing the expression of numerous glycolytic enzymes that are isoforms of those found in non-malignant cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6941045PMC
http://dx.doi.org/10.3390/ijms20246140DOI Listing

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