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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.