PMID- 16002209
OWN - NLM
STAT- MEDLINE
DCOM- 20060726
LR  - 20061115
IS  - 0304-3835 (Print)
IS  - 0304-3835 (Linking)
VI  - 237
IP  - 1
DP  - 2006 Jun 8
TI  - Tumor hypoxia and cancer progression.
PG  - 10-21
AB  - Aerobic life consumes oxygen for efficient production of high energy compounds. 
      The ability to sense and respond to changes in oxygen partial pressure represents 
      a fundamental property to assure the cellular oxygen supply to be within a narrow 
      range that balances the risks of oxidative damage vs. oxygen deficiency. The 
      discovery of hypoxia-inducible factor-1 (HIF-1) allowed the identification of 
      molecular mechanisms by which changes in oxygenation are transduced to adequate 
      intracellular adaptive responses. It became apparent that hypoxia can initiate 
      cell demise by apoptosis/necrosis but also prevent cell death by provoking 
      adaptive responses that, in turn, facilitate cell proliferation or angiogenesis, 
      thus contributing to tumor progression. Considering that activation of HIF-1 
      provokes pro-survival as well as pro-death decisions under hypoxia, it will be 
      crucial to understand decision making processes in regulating cell death, 
      adaptation and chemoresistance. Likely, secondary stressors such as pH changes, 
      i.e. acidosis, and the context of genetic alterations will shape the role of 
      HIF-1 to affect susceptibility of cells to undergo hypoxia-induced cell death or 
      to allow adaptation and progression towards malignancy. Understanding the 
      mechanisms by which HIF-1 affects the expression and/or function of key apoptotic 
      regulators such as Bcl-2 family members or p53 will help to uncover how HIF-1 
      induces cell death and the manner in which cells can overcome such signals and 
      thus determine which of its Janus faces prevail.
FAU - Zhou, Jie
AU  - Zhou J
AD  - Institute of Biochemistry I, Faculty of Medicine, Johann Wolfgang 
      Goethe-University, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
FAU - Schmid, Tobias
AU  - Schmid T
FAU - Schnitzer, Steffen
AU  - Schnitzer S
FAU - Brune, Bernhard
AU  - Brune B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20050705
PL  - Ireland
TA  - Cancer Lett
JT  - Cancer letters
JID - 7600053
RN  - 0 (Angiogenic Proteins)
RN  - 0 (BNIP3 protein, human)
RN  - 0 (BNIP3L protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Membrane Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 138391-32-9 (Aryl Hydrocarbon Receptor Nuclear Translocator)
SB  - IM
MH  - Angiogenic Proteins/genetics/metabolism
MH  - Animals
MH  - Apoptosis/*genetics
MH  - Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism
MH  - Cell Hypoxia/*genetics
MH  - Cell Proliferation
MH  - Disease Progression
MH  - Drug Resistance, Neoplasm/genetics
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
MH  - Membrane Proteins/genetics/metabolism
MH  - Neoplasms/blood supply/*genetics/metabolism
MH  - Neovascularization, Pathologic/genetics/metabolism
MH  - Proto-Oncogene Proteins/genetics/metabolism
MH  - Tumor Suppressor Protein p53/genetics/metabolism
MH  - Tumor Suppressor Proteins/genetics/metabolism
RF  - 67
EDAT- 2005/07/09 09:00
MHDA- 2006/07/27 09:00
CRDT- 2005/07/09 09:00
PHST- 2005/05/16 00:00 [received]
PHST- 2005/05/23 00:00 [revised]
PHST- 2005/05/24 00:00 [accepted]
PHST- 2005/07/09 09:00 [pubmed]
PHST- 2006/07/27 09:00 [medline]
PHST- 2005/07/09 09:00 [entrez]
AID - S0304-3835(05)00511-2 [pii]
AID - 10.1016/j.canlet.2005.05.028 [doi]
PST - ppublish
SO  - Cancer Lett. 2006 Jun 8;237(1):10-21. doi: 10.1016/j.canlet.2005.05.028. Epub 
      2005 Jul 5.