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The 2-oxoglutarate carrier promotes liver cancer by sustaining mitochondrial GSH despite cholesterol loading. | LitMetric

The 2-oxoglutarate carrier promotes liver cancer by sustaining mitochondrial GSH despite cholesterol loading.

Redox Biol

Department of Cell Death and Proliferation, Instituto de Investigaciones Biomédicas de Barcelona, Consejo Superior de Investigaciones Científicas, 08036 Barcelona, Spain; Liver Unit and Hospital Clínic i Provincial, IDIBAPS, and Centro de Investigación Biomédica en Red (CIBERehd), Spain; Southern California Research Center for ALPD and Cirrhosis, Los Angeles, CA, USA; University of Southern California Research Center for Liver Diseases, Keck School of Medicine, USC, Los Angeles, CA, USA. Electronic address:

Published: April 2018

AI Article Synopsis

  • Cancer cells accumulate mitochondrial cholesterol (mt-cholesterol), which helps them resist cell death by preventing damage to the mitochondrial outer membrane, but this accumulation can also lead to liver disease and depletion of important antioxidants.
  • Research showed that hepatocellular carcinoma (HCC) cells selectively upregulate a mitochondrial carrier called SLC25A11 (2-oxoglutarate carrier, OGC) to maintain levels of mitochondrial GSH (mGSH) even when mt-cholesterol is high.
  • Silencing OGC led to decreased mGSH levels and increased cell death from stress, suggesting that OGC plays a critical role in supporting HCC cells and may be a potential target for new cancer therapies.

Article Abstract

Cancer cells exhibit mitochondrial cholesterol (mt-cholesterol) accumulation, which contributes to cell death resistance by antagonizing mitochondrial outer membrane (MOM) permeabilization. Hepatocellular mt-cholesterol loading, however, promotes steatohepatitis, an advanced stage of chronic liver disease that precedes hepatocellular carcinoma (HCC), by depleting mitochondrial GSH (mGSH) due to a cholesterol-mediated impairment in mGSH transport. Whether and how HCC cells overcome the restriction of mGSH transport imposed by mt-cholesterol loading to support mGSH uptake remains unknown. Although the transport of mGSH is not fully understood, SLC25A10 (dicarboxylate carrier, DIC) and SLC25A11 (2-oxoglutarate carrier, OGC) have been involved in mGSH transport, and therefore we examined their expression and role in HCC. Unexpectedly, HCC cells and liver explants from patients with HCC exhibit divergent expression of these mitochondrial carriers, with selective OGC upregulation, which contributes to mGSH maintenance. OGC but not DIC downregulation by siRNA depleted mGSH levels and sensitized HCC cells to hypoxia-induced ROS generation and cell death as well as impaired cell growth in three-dimensional multicellular HCC spheroids, effects that were reversible upon mGSH replenishment by GSH ethyl ester, a membrane permeable GSH precursor. We also show that OGC regulates mitochondrial respiration and glycolysis. Moreover, OGC silencing promoted hypoxia-induced cardiolipin peroxidation, which reversed the inhibition of cholesterol on the permeabilization of MOM-like liposomes induced by Bax or Bak. Genetic OGC knockdown reduced the ability of tumor-initiating stem-like cells to induce liver cancer. These findings underscore the selective overexpression of OGC as an adaptive mechanism of HCC to provide adequate mGSH levels in the face of mt-cholesterol loading and suggest that OGC may be a novel therapeutic target for HCC treatment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609874PMC
http://dx.doi.org/10.1016/j.redox.2017.08.022DOI Listing

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