Evidence map›Paper›PMID 23644529›Full record

ReviewCancer research2013

AMPK: a contextual oncogene or tumor suppressor?

Jiyong Liang, Gordon B Mills

Open access · greenAbstract readReview
In one paragraph

Review in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed
15.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

168 citing papers in PubMed, 248 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Energy Metabolism Profiling of Human Colorectal Tumours.Journal of cellular and molecular medicine · 2025
    Article
  10. Review
  11. Article
  12. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

108 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jiyong LiangSystems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. jyliang@mdanderson.org
Gordon B Mills
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
NCI NIH HHS P01 CA099031NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

The AMP-activated protein kinase (AMPK) functions to monitor and maintain energy homeostasis at the cellular and organism level. AMPK was 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 AMPK is required for oncogenic transformation. Thus, whether AMPK acts as a bona fide tumor suppressor or a contextual oncogene and, of particular importance, whether AMPK should 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.

Indexed as

OncogenesAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsHoloenzymesHumansPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTumor Suppressor ProteinsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesHoloenzymesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSTK11 protein, humanTumor Suppressor Proteins

Identifiers

PMID23644529
PMCPMC3725287
OpenAlexW2141574380

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.