AMPK

A contextual oncogene or tumor suppressor?

Jiyong Liang, Gordon Mills

Research output: Contribution to journalReview article

150 Citations (Scopus)

Abstract

The AMP-activated protein kinase (AMPK) functions to monitor and maintain energy homeostasis at the cellular and organism level. AMPKwas perceived historically primarily as a component of the LKB1/STK11 tumor suppressor (LKB1 mutations cause the Peutz-Jegher cancer predisposition syndrome) cascade upstream of the TSC1/2/mTOR pathway and thus likely to be a tumor suppressor. However, AMPK has recently been shown to promote cancer cell survival in the face of extrinsic and intrinsic stressors including bioenergetic, growth factor, and oncogene stress compatible with studies showing that AMPKis required for oncogenic transformation. Thus, whether AMPK acts as a bona fide tumor suppressor or a contextual oncogene and, of particular importance, whether AMPKshould be targeted for activation or inhibition during cancer therapy, is controversial and requires clarification. We aim to initiate discussions of these critical questions by reviewing the role of AMPK with an emphasis on cancer cell adaptation to microenvironment stress and therapeutic intervention. Cancer Res; 73(10); 2929-35.

Original languageEnglish (US)
Pages (from-to)2929-2935
Number of pages7
JournalCancer Research
Volume73
Issue number10
DOIs
StatePublished - May 15 2013
Externally publishedYes

Fingerprint

AMP-Activated Protein Kinases
Cyclic AMP-Dependent Protein Kinases
Oncogenes
Neoplasms
Genetic Suppression
Energy Metabolism
Cell Survival
Intercellular Signaling Peptides and Proteins
Homeostasis
Therapeutics

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

AMPK : A contextual oncogene or tumor suppressor? / Liang, Jiyong; Mills, Gordon.

In: Cancer Research, Vol. 73, No. 10, 15.05.2013, p. 2929-2935.

Research output: Contribution to journalReview article

Liang, Jiyong ; Mills, Gordon. / AMPK : A contextual oncogene or tumor suppressor?. In: Cancer Research. 2013 ; Vol. 73, No. 10. pp. 2929-2935.
@article{5c9d7c33da1f4d41a3762836f4baf23d,
title = "AMPK: A contextual oncogene or tumor suppressor?",
abstract = "The AMP-activated protein kinase (AMPK) functions to monitor and maintain energy homeostasis at the cellular and organism level. AMPKwas perceived historically primarily as a component of the LKB1/STK11 tumor suppressor (LKB1 mutations cause the Peutz-Jegher cancer predisposition syndrome) cascade upstream of the TSC1/2/mTOR pathway and thus likely to be a tumor suppressor. However, AMPK has recently been shown to promote cancer cell survival in the face of extrinsic and intrinsic stressors including bioenergetic, growth factor, and oncogene stress compatible with studies showing that AMPKis required for oncogenic transformation. Thus, whether AMPK acts as a bona fide tumor suppressor or a contextual oncogene and, of particular importance, whether AMPKshould be targeted for activation or inhibition during cancer therapy, is controversial and requires clarification. We aim to initiate discussions of these critical questions by reviewing the role of AMPK with an emphasis on cancer cell adaptation to microenvironment stress and therapeutic intervention. Cancer Res; 73(10); 2929-35.",
author = "Jiyong Liang and Gordon Mills",
year = "2013",
month = "5",
day = "15",
doi = "10.1158/0008-5472.CAN-12-3876",
language = "English (US)",
volume = "73",
pages = "2929--2935",
journal = "Journal of Cancer Research",
issn = "0099-7013",
publisher = "American Association for Cancer Research Inc.",
number = "10",

}

TY - JOUR

T1 - AMPK

T2 - A contextual oncogene or tumor suppressor?

AU - Liang, Jiyong

AU - Mills, Gordon

PY - 2013/5/15

Y1 - 2013/5/15

N2 - The AMP-activated protein kinase (AMPK) functions to monitor and maintain energy homeostasis at the cellular and organism level. AMPKwas perceived historically primarily as a component of the LKB1/STK11 tumor suppressor (LKB1 mutations cause the Peutz-Jegher cancer predisposition syndrome) cascade upstream of the TSC1/2/mTOR pathway and thus likely to be a tumor suppressor. However, AMPK has recently been shown to promote cancer cell survival in the face of extrinsic and intrinsic stressors including bioenergetic, growth factor, and oncogene stress compatible with studies showing that AMPKis required for oncogenic transformation. Thus, whether AMPK acts as a bona fide tumor suppressor or a contextual oncogene and, of particular importance, whether AMPKshould be targeted for activation or inhibition during cancer therapy, is controversial and requires clarification. We aim to initiate discussions of these critical questions by reviewing the role of AMPK with an emphasis on cancer cell adaptation to microenvironment stress and therapeutic intervention. Cancer Res; 73(10); 2929-35.

AB - The AMP-activated protein kinase (AMPK) functions to monitor and maintain energy homeostasis at the cellular and organism level. AMPKwas perceived historically primarily as a component of the LKB1/STK11 tumor suppressor (LKB1 mutations cause the Peutz-Jegher cancer predisposition syndrome) cascade upstream of the TSC1/2/mTOR pathway and thus likely to be a tumor suppressor. However, AMPK has recently been shown to promote cancer cell survival in the face of extrinsic and intrinsic stressors including bioenergetic, growth factor, and oncogene stress compatible with studies showing that AMPKis required for oncogenic transformation. Thus, whether AMPK acts as a bona fide tumor suppressor or a contextual oncogene and, of particular importance, whether AMPKshould be targeted for activation or inhibition during cancer therapy, is controversial and requires clarification. We aim to initiate discussions of these critical questions by reviewing the role of AMPK with an emphasis on cancer cell adaptation to microenvironment stress and therapeutic intervention. Cancer Res; 73(10); 2929-35.

UR - http://www.scopus.com/inward/record.url?scp=84877851087&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84877851087&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-12-3876

DO - 10.1158/0008-5472.CAN-12-3876

M3 - Review article

VL - 73

SP - 2929

EP - 2935

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0099-7013

IS - 10

ER -