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Publication Detail
SCaMC-1 promotes cancer cell survival by desensitizing mitochondrial permeability transition via ATP/ADP-mediated matrix Ca(2+) buffering.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Traba J, Del Arco A, Duchen MR, Szabadkai G, Satrústegui J
  • Publication date:
    04/2012
  • Pagination:
    650, 660
  • Journal:
    Cell Death Differ
  • Volume:
    19
  • Issue:
    4
  • Status:
    Published
  • Country:
    England
  • PII:
    cdd2011139
  • Language:
    eng
  • Keywords:
    Adenosine Diphosphate, Adenosine Triphosphate, Animals, COS Cells, Calcium, Calcium-Binding Proteins, Cell Line, Tumor, Cell Survival, Chlorocebus aethiops, Mice, Mitochondria, Necrosis, Neoplasms, Oxidative Stress, Permeability
Abstract
Ca(2+)-mediated mitochondrial permeability transition (mPT) is the final common pathway of stress-induced cell death in many major pathologies, but its regulation in intact cells is poorly understood. Here we report that the mitochondrial carrier SCaMC-1/SLC25A24 mediates ATP-Mg(2-)/Pi(2-) and/or HADP(2-)/Pi(2-) uptake into the mitochondria after an increase in cytosolic [Ca(2+)]. ATP and ADP contribute to Ca(2+) buffering in the mitochondrial matrix, resulting in desensitization of the mPT. Comprehensive gene expression analysis showed that SCaMC-1 overexpression is a general feature of transformed and cancer cells. Knockdown of the transporter led to vast reduction of mitochondrial Ca(2+) buffering capacity and sensitized cells to mPT-mediated necrotic death triggered by oxidative stress and Ca(2+) overload. These findings revealed that SCaMC-1 exerts a negative feedback control between cellular Ca(2+) overload and mPT-dependent cell death, suggesting that the carrier might represent a novel target for cancer therapy.
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