Abstract
// Noel A. Warfel 1 , 2 1 University of Arizona Cancer Center, Tucson, AZ, USA 2 Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, USA Correspondence to: Noel A. Warfel, email: warfelna@arizona.edu Keywords: hypoxia; HIF-1; cyclin dependent kinase; SMURF2 Received: October 26, 2021     Accepted: February 15, 2022     Published: March 03, 2022 Copyright: © 2022 Warfel. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Highlights
Constitutive activation of HIF-1α is common in human cancers, regardless of oxygen tension
Stabilization of HIF-1α in normoxia has been attributed to genetic alterations, most notably loss of the von Hippel-Lindau (VHL) tumor suppressor gene, the primary E3 ligase responsible for targeting HIF-1α for proteasomal degradation [1]
Prior research from the El-Deiry lab was the first to demonstrate that the cyclin dependent kinases CDK1 and CDK4/6 are sufficient to stabilize HIF-1α, independent of hypoxia or VHL
Summary
Constitutive activation of HIF-1α is common in human cancers, regardless of oxygen tension. While the majority of HIF-1 activation can be attributed to lack of oxygen in the tumor microenvironment, numerous nonhypoxic stimuli have been shown to regulate HIF1α levels.
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