PMID- 28327594
OWN - NLM
STAT- MEDLINE
DCOM- 20181108
LR  - 20181113
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 7
DP  - 2017 Mar 22
TI  - Aspirin induces cell death by directly modulating mitochondrial voltage-dependent 
      anion channel (VDAC).
PG  - 45184
LID - 10.1038/srep45184 [doi]
LID - 45184
AB  - 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 (Deltapsi(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.
FAU - Tewari, Debanjan
AU  - Tewari D
AD  - Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences 
      Building, Indian Institute of Technology Madras, Chennai 600036, India.
FAU - Majumdar, Dhriti
AU  - Majumdar D
AD  - Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences 
      Building, Indian Institute of Technology Madras, Chennai 600036, India.
FAU - Vallabhaneni, Sirisha
AU  - Vallabhaneni S
AD  - Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences 
      Building, Indian Institute of Technology Madras, Chennai 600036, India.
FAU - Bera, Amal Kanti
AU  - Bera AK
AD  - Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences 
      Building, Indian Institute of Technology Madras, Chennai 600036, India.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170322
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 1.6.- (Voltage-Dependent Anion Channel 1)
RN  - EC 2.7.1.1 (Hexokinase)
RN  - R16CO5Y76E (Aspirin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Aspirin/*pharmacology
MH  - Calcium/metabolism
MH  - HeLa Cells
MH  - Hexokinase/metabolism
MH  - Humans
MH  - Membrane Potential, Mitochondrial
MH  - Mitochondria/*drug effects/metabolism
MH  - Rats
MH  - Voltage-Dependent Anion Channel 1/*metabolism
PMC - PMC5361111
COIS- The authors declare no competing financial interests.
EDAT- 2017/03/23 06:00
MHDA- 2018/11/09 06:00
PMCR- 2017/03/22
CRDT- 2017/03/23 06:00
PHST- 2015/07/20 00:00 [received]
PHST- 2017/02/20 00:00 [accepted]
PHST- 2017/03/23 06:00 [entrez]
PHST- 2017/03/23 06:00 [pubmed]
PHST- 2018/11/09 06:00 [medline]
PHST- 2017/03/22 00:00 [pmc-release]
AID - srep45184 [pii]
AID - 10.1038/srep45184 [doi]
PST - epublish
SO  - Sci Rep. 2017 Mar 22;7:45184. doi: 10.1038/srep45184.