PMID- 22204343
OWN - NLM
STAT- MEDLINE
DCOM- 20120723
LR  - 20190823
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Linking)
VI  - 19
IP  - 5
DP  - 2012
TI  - Mitochondrial VDAC1: function in cell life and death and a target for cancer 
      therapy.
PG  - 714-35
AB  - Found at the outer mitochondrial membrane, the voltage-dependent anion channel, 
      VDAC, assumes a crucial position in the cell, serving as the main interface 
      between mitochondrial and cellular metabolisms by mediating transport of ions and 
      metabolites. VDAC thus functions as a gatekeeper, controlling cross-talk between 
      mitochondria and the rest of the cell. Moreover, its location at the boundary 
      between the mitochondria and the cytosol enables VDAC to interact with proteins 
      that mediate and regulate the integration of mitochondrial functions with other 
      cellular activities. Here, we review current knowledge related to the roles 
      played by VDAC in the regulation of cell life and cell death, with relation to 
      cancer. The current concepts of altered metabolism in cancer cells are presented 
      with specific emphasis on mitochondrial, more specifically VDAC1-bound hexokinase 
      (HK), facilitating and promoting the high glycolytic tumor phenotype. In this 
      respect, the up-regulation of HK expression in tumor cells and its binding to 
      VDAC provide both a metabolic benefit and apoptosis-suppressive capacity that 
      offers the cell a growth advantage and increases its resistance to chemotherapy. 
      VDAC has also been recognized as a key protein in mitochondria-mediated apoptosis 
      since it is the proposed target for the pro- and antiapoptotic Bcl-2-family of 
      proteins, as well as due to its function in the release of apoptotic proteins 
      located in the inter-membranal space. These and other functions point to VDAC1 as 
      being a rational target for the development of a new generation of therapeutics.
FAU - Shoshan-Barmatz, V
AU  - Shoshan-Barmatz V
AD  - Department of Life Sciences, Ben-Gurion University of the Negev, Beer Sheva 
      84105, Israel. vardasb@bgu.ac.il
FAU - Golan, M
AU  - Golan M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - EC 1.6.- (Voltage-Dependent Anion Channel 1)
RN  - EC 2.7.1.1 (Hexokinase)
SB  - IM
MH  - Apoptosis Regulatory Proteins
MH  - Cell Survival
MH  - Hexokinase/metabolism
MH  - Humans
MH  - Mitochondrial Proteins/physiology
MH  - Molecular Targeted Therapy
MH  - Neoplasms/*drug therapy/metabolism/pathology
MH  - Voltage-Dependent Anion Channel 1/antagonists & inhibitors/*drug 
      effects/physiology
EDAT- 2011/12/30 06:00
MHDA- 2012/07/24 06:00
CRDT- 2011/12/30 06:00
PHST- 2011/08/24 00:00 [received]
PHST- 2011/10/20 00:00 [accepted]
PHST- 2011/12/30 06:00 [entrez]
PHST- 2011/12/30 06:00 [pubmed]
PHST- 2012/07/24 06:00 [medline]
AID - BSP/CMC/E-Pub/2012/058 [pii]
AID - 10.2174/092986712798992110 [doi]
PST - ppublish
SO  - Curr Med Chem. 2012;19(5):714-35. doi: 10.2174/092986712798992110.