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10.1038/srep45184

http://scihub22266oqcxt.onion/10.1038/srep45184
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suck abstract from ncbi


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pmid28327594
      Sci+Rep 2017 ; 7 (ä): 45184
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  • Aspirin induces cell death by directly modulating mitochondrial voltage-dependent anion channel (VDAC) #MMPMID28327594
  • Tewari D ; Majumdar D ; Vallabhaneni S ; Bera AK
  • Sci Rep 2017[Mar]; 7 (ä): 45184 PMID28327594 show ga
  • Aspirin induces apoptotic cell death in various cancer cell lines. Here we showed that silencing of VDAC1 protected HeLa cells from aspirin-induced cell death. Compared to the wild type cells, VDAC1 knocked down cells showed lesser change of mitochondrial membrane potential (??(m)), upon aspirin treatment. Aspirin augmented ATP and ionomycin-induced mitochondrial Ca(2+) uptake which was abolished in VDAC1 knocked down cells. Aspirin dissociated bound hexokinase II (HK-II) from mitochondria. Further, aspirin promoted the closure of recombinant human VDAC1, reconstituted in planar lipid bilayer. Taken together, these results imply that VDAC1 serves as a novel target for aspirin. Modulation of VDAC1 is possibly associated with the cell death and anticancer effects of aspirin.
  • |Adenosine Triphosphate/metabolism [MESH]
  • |Animals [MESH]
  • |Anti-Inflammatory Agents, Non-Steroidal/*pharmacology [MESH]
  • |Apoptosis/*drug effects [MESH]
  • |Aspirin/*pharmacology [MESH]
  • |Calcium/metabolism [MESH]
  • |HeLa Cells [MESH]
  • |Hexokinase/metabolism [MESH]
  • |Humans [MESH]
  • |Membrane Potential, Mitochondrial [MESH]
  • |Mitochondria/*drug effects/metabolism [MESH]
  • |Rats [MESH]


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