Aspirin induces cell death by directly modulating mitochondrial voltage-dependent anion channel (VDAC)

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 Ca2+ 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.

DOI: 10.1038/srep45184

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@inproceedings{Tewari2017AspirinIC, title={Aspirin induces cell death by directly modulating mitochondrial voltage-dependent anion channel (VDAC)}, author={Debanjan Tewari and Dhriti Majumdar and Sirisha Vallabhaneni and Amal Kanti Bera}, booktitle={Scientific reports}, year={2017} }