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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.