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. Author manuscript; available in PMC: 2024 Jul 2.
Published in final edited form as: Cancer Lett. 2020 Aug 18;493:71–79. doi: 10.1016/j.canlet.2020.06.013

Figure 1. Lipolytic inhibition by HIG2 is central for a survival strategy employed by hypoxic cancer cells.

Figure 1.

(A) In normoxic cells where HIF-1α protein stability is low due to increased ubiquitination and proteasomal degradation, ATGL-mediated lipolysis is active and downstream FA oxidation contributes to the overall energy production. (B) Hypoxic stabilization of HIF-1α protein leads to expression of the ATGL inhibitor HIG2, and subsequent lipolytic inhibition results in decreased FA oxidation along with improved oxygen homeostasis and cell viability. (C) HIG2 deficiency, induced either genetically or pharmacologically, forces increased lipolysis and FA oxidation that exacerbate ROS generation and apoptotic death in hypoxic cancer cells.