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Aspirin induces cell death by directly modulating mitochondrial voltage-dependent anion channel (VDAC)
Dhriti Majumdar, Sirisha Vallabhaneni,
Published in Nature Publishing Group
2017
PMID: 28327594
Volume: 7
   
Abstract
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 (δψm), 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. © The Author(s) 2017.
About the journal
JournalScientific Reports
PublisherNature Publishing Group
ISSN20452322
Open AccessYes
Concepts (25)
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    ACETYLSALICYLIC ACID
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    Adenosine triphosphate
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    Calcium
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    HEXOKINASE
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    NONSTEROID ANTIINFLAMMATORY AGENT
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    VOLTAGE DEPENDENT ANION CHANNEL 1
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    Animal
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    Apoptosis
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    Drug effect
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    Hela cell line
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    Human
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    Metabolism
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    Mitochondrial membrane potential
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    Mitochondrion
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    Rat
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    Animals
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    ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL
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    Aspirin
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    Hela cells
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    HEXOKINASE
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    Humans
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    Membrane potential, mitochondrial
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    Mitochondria
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    Rats
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    VOLTAGE-DEPENDENT ANION CHANNEL 1