SIRT3 Controls Cancer Metabolic Reprogramming by Regulating ROS and HIF

Paul T. Schumacker

doi:10.1016/j.ccr.2011.03.001

SIRT3 Controls Cancer Metabolic Reprogramming by Regulating ROS and HIF

Paul T. Schumacker^*

^*Corresponding author for this work

Pediatrics

Research output: Contribution to journal › Short survey › peer-review

57 Scopus citations

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.

Original language	English (US)
Pages (from-to)	299-300
Number of pages	2
Journal	Cancer Cell
Volume	19
Issue number	3
DOIs	https://doi.org/10.1016/j.ccr.2011.03.001
State	Published - Mar 8 2011

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.ccr.2011.03.001

Cite this

@article{b4bbd35a71a84850be2c918cd973009e,

title = "SIRT3 Controls Cancer Metabolic Reprogramming by Regulating ROS and HIF",

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.",

author = "Schumacker, {Paul T.}",

year = "2011",

month = mar,

day = "8",

doi = "10.1016/j.ccr.2011.03.001",

language = "English (US)",

volume = "19",

pages = "299--300",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "3",

}

TY - JOUR

T1 - SIRT3 Controls Cancer Metabolic Reprogramming by Regulating ROS and HIF

AU - Schumacker, Paul T.

PY - 2011/3/8

Y1 - 2011/3/8

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=79952523493&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79952523493&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2011.03.001

DO - 10.1016/j.ccr.2011.03.001

M3 - Short survey

C2 - 21397853

AN - SCOPUS:79952523493

VL - 19

SP - 299

EP - 300

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 3

ER -

SIRT3 Controls Cancer Metabolic Reprogramming by Regulating ROS and HIF

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this