Evidence map›Paper›PMID 25812084›Full record

ReviewOncotarget2015

Targeting AMPK for cancer prevention and treatment.

Weidong Li, Shakir M Saud, Matthew R Young, Guohong Chen, Baojin Hua

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 3 pooled it
15.4field-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

196 citing papers in PubMed, 3 syntheses or guidelines pooled it, 356 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Review
  7. Article
  8. AMPK Limits MNNG-Induced Parthanatos by Inhibiting BH3-Only Protein Bim.International journal of molecular sciences · 2025
    Article
  9. Review
  10. Article
  11. Evolutionary Transcriptomics of Cancer Development.International journal of molecular sciences · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

136 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

5 authors at 5 institutions in 2 countries.

Weidong LiDepartment of Oncology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Shakir M SaudNutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
Matthew R YoungBasic Research Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA.
Guohong ChenDepartment of Urinary Surgery, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Baojin HuaDepartment of Oncology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Center for Cancer Research · USChinese Academy of Medical Sciences & Peking Union Medical College · CNFrederick National Laboratory for Cancer Research · USGuang’anmen Hospital · CNNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is an important mediator in maintaining cellular energy homeostasis. AMPK is activated in response to a shortage of energy. Once activated, AMPK can promote ATP production and regulate metabolic energy. AMPK is a known target for treating metabolic syndrome and type-2 diabetes; however, recently AMPK is emerging as a possible metabolic tumor suppressor and target for cancer prevention and treatment. Recent epidemiological studies indicate that treatment with metformin, an AMPK activator reduces the incidence of cancer. In this article we review the role of AMPK in regulating inflammation, metabolism, and other regulatory processes with an emphasis on cancer, as well as, discuss the potential for targeting AMPK to treat various types of cancer. Activation of AMPK has been found to oppose tumor progression in several cancer types and offers a promising cancer therapy. This review evaluates the evidence linking AMPK with tumor suppressor function and analyzes the molecular mechanisms involved. AMPK activity opposes tumor development and progression in part by regulating inflammation and metabolism.

Indexed as

AMP-Activated Protein KinasesAnimalsHumansMolecular Targeted TherapyNeoplasmsSignal TransductionAMP-Activated Protein KinasesAMP activated kinasecancerpreventiontreatment

Identifiers

PMID25812084
PMCPMC4480686
OpenAlexW1495274944

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.