SIRT3 controls cancer metabolic reprogramming by regulating ROS and HIF.

Cancer cell ·Vol. 19 ·No. 3 ·2011-03-08 ·Pages 299-300

Schumacker PT

Abstract

In this issue of Cancer Cell, Finley and coworkers report that the genetic loss of the deacetylase SIRT3 leads to metabolic reprogramming toward glycolysis. This shift is mediated by an increase in cellular reactive oxygen species (ROS) generation that amplifies HIF-α stabilization and HIF-dependent gene expression, thereby driving the tumor phenotype.

MeSH Terms

Animals Cell Line, Tumor Cells, Cultured Fibroblasts/cytology,metabolism Glucose/metabolism Glycolysis Humans Hypoxia-Inducible Factor 1, alpha Subunit/metabolism Metabolomics/methods Mice Mice, Knockout Models, Biological Neoplasms/genetics,metabolism,pathology Reactive Oxygen Species/metabolism Sirtuin 3/genetics,metabolism

Chemicals

Hypoxia-Inducible Factor 1, alpha Subunit Reactive Oxygen Species SIRT3 protein, human Sirtuin 3 Glucose

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Schumacker Paul T

Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E. Superior St. Searle Bldg. 4-685, Chicago, IL 60611, USA. [email protected]

References (9)

9 references, click to expand

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Article Info

Journal

Cancer cell

Abbr.

Cancer Cell

ISSN

1878-3686

DOI

10.1016/j.ccr.2011.03.001

[email protected]

Published

2011-03-08

Pages

299-300

Language

English

Region

United States

NLM ID

101130617

PMCID

PMC3087169

Subset

Grants

NHLBI NIH HHS · R01 HL079650-05 · United States

NHLBI NIH HHS · R01 HL035440-24 · United States

NHLBI NIH HHS · R01 HL079650 · United States

NHLBI NIH HHS · R01 HL035440 · United States

NHLBI NIH HHS · R01 HL035440-25 · United States

Corrections

CommentOn

PMID: 21397863

External Links

PubMed source DOI: 10.1016/j.ccr.2011.03.001 PMC Full Text View journal details

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SIRT3 controls cancer metabolic reprogramming by regulating ROS and HIF.

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