Evidence map›Paper›PMID 23859619›Full record

ReviewCurrent pharmaceutical design2014

AMPK as a potential anticancer target - friend or foe?

Hsiao-Ching Chuang, Chih-Chien Chou, Samuel K Kulp, Ching-Shih Chen

Open access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Integrative Analysis of the AMPK subunits in Colorectal Adeno Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Hsiao-Ching Chuang
Chih-Chien Chou
Samuel K Kulp
Ching-Shih ChenRm 336, Parks Hall, College of Pharmacy, The Ohio State University, 500 W. 12th Avenue, Columbus, OH 43210, USA. chen.844@osu.edu.
The Ohio State University · US

Funding

Targeting Akt and Bcl-2 in Prostate Cancer PreventionR01CA112250 · NCI · OHIO STATE UNIVERSITY · PI CHEN, CHING-SHIH · 2005 to 2015
$2.8M
Novel AMPK Activators in Breast Cancer PreventionR21CA158807 · NCI · OHIO STATE UNIVERSITY · PI CHEN, CHING-SHIH · 2011 to 2012
$365k
NCI NIH HHS R01 CA112250NCI NIH HHS R01CA112250NCI NIH HHS R21 CA158807NCI NIH HHS R21CA158807
6 · The paper itself

Abstract

Adenosine monophosphate-activated protein kinase (AMPK) is a key player in maintaining energy homeostasis in response to metabolic stress. Beyond diabetes and metabolic syndrome, there is a growing interest in the therapeutic exploitation of the AMPK pathway in cancer treatment in light of its unique ability to regulate cancer cell proliferation through the reprogramming of cell metabolism. Although many studies support the tumor-suppressive role of AMPK, emerging evidence suggests that the metabolic checkpoint function of AMPK might be overridden by stress or oncogenic signals so that tumor cells use AMPK activation as a survival strategy to gain growth advantage. These findings underscore the complexity in the cellular function of AMPK in maintaining energy homeostasis under physiological versus pathological conditions. Thus, this review aims to provide an overview of recent findings on the functional interplay of AMPK with different cell metabolic and signaling effectors, particularly histone deacetylases, in mediating downstream tumor suppressive or promoting mechanisms in different cell systems. Although AMPK activation inhibits tumor growth by targeting multiple signaling pathways relevant to tumorigenesis, under certain cellular contexts or certain stages of tumor development, AMPK might act as a protective response to metabolic stresses, such as nutrient deprivation, low oxygen, and low pH, or as downstream effectors of oncogenic proteins, including androgen receptor, hypoxia-inducible factor-1α, c-Src, and MYC. Thus, investigations to define at which stage(s) of tumorigenesis and cancer progression or for which genetic aberrations AMPK inhibition might represent a more relevant strategy than AMPK activation for cancer treatment are clearly warranted.

Indexed as

AMP-Activated Protein KinasesAnimalsAutophagyEnzyme ActivationGene Expression RegulationHistone DeacetylasesHumansNeoplasmsPhosphorylationProtein Kinase InhibitorsAMP-Activated Protein KinasesHistone DeacetylasesProtein Kinase Inhibitors

Identifiers

PMID23859619
PMCPMC4264967
OpenAlexW126783609

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.