Regulation of cancer cell metabolism by hypoxia-inducible factor 1

Abstract The induction of hypoxia-inducible factor 1 (HIF-1) activity, either as a result of intratumoral hypoxia or loss-of-function mutations in the VHL gene, leads to a dramatic reprogramming of cancer cell metabolism involving increased glucose transport into the cell, increased conversion of gl...

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Bibliographic Details
Published in:Seminars in cancer biology 2009-02, Vol.19 (1), p.12-16
Main Author: Semenza, Gregg L
Format: Article
Language:English
Subjects:
Animals
BNIP3
Cell Hypoxia - physiology
Gene Expression Regulation, Neoplastic
Glucose transporter
Glycolysis
Glycolysis - physiology
Hematology, Oncology and Palliative Medicine
HIF-1
Humans
Hypoxia-Inducible Factor 1 - genetics
Hypoxia-Inducible Factor 1 - metabolism
Lactate dehydrogenase
MCT4
Metabolic Networks and Pathways - physiology
Mitochondrial autophagy
Neoplasms - enzymology
Neoplasms - genetics
Neoplasms - metabolism
NHE1
Oxygen
PDK1
Reactive Oxygen Species - metabolism
Von Hippel-Lindau Tumor Suppressor Protein - metabolism
Warburg effect
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Summary:Abstract The induction of hypoxia-inducible factor 1 (HIF-1) activity, either as a result of intratumoral hypoxia or loss-of-function mutations in the VHL gene, leads to a dramatic reprogramming of cancer cell metabolism involving increased glucose transport into the cell, increased conversion of glucose to pyruvate, and a concomitant decrease in mitochondrial metabolism and mitochondrial mass. Blocking these adaptive metabolic responses to hypoxia leads to cell death due to toxic levels of reactive oxygen species. Targeting HIF-1 or metabolic enzymes encoded by HIF-1 target genes may represent a novel therapeutic approach to cancer.
ISSN:1044-579X
1096-3650
DOI:10.1016/j.semcancer.2008.11.009