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HIF-1-Regulated Glucose Metabolism: A Key to Apoptosis Resistance?

Simone Fulda and Klaus-Michael Debatin

volume 6 | issue 7

1 April 2007
Pages: 790 - 792

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Resistance of human cancers to current treatment regimens remains a challenge in oncology. Therefore, there has been much interest in identifying molecular pathways that are responsible for primary or acquired resistance of cancers. Hypoxia is a characteristic feature of most solid tumors and has been associated with poor treatment response. In response to hypoxia cancer cells undergo a variety of adoptive changes including activation of signaling pathways, which promote cancer cell survival and block cell death. Hypoxia inducible factor-1 (HIF-1) is the major transcription factor that mediates adaptation of cancer cells to the hypoxic environment. There is mounting evidence that Hif-1α, the oxygen sensitive subunit of HIF-1, provides protection against cell death and stimulates tumor growth by upregulating genes that are involved in cellular energy metabolism. Thus, Hif-1α and hypoxia-inducible genes represent attractive targets for the development of pharmacological inhibitors, which may offer new therapeutic options for a wide range of adult and also pediatric malignancies.

Authors

Simone Fulda

University Children’s Hospital; Ulm, Germany

Klaus-Michael Debatin

University Children’s Hospital; Ulm, Germany



We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.