Evidence map›Paper›PMID 33862221›Full record

ReviewSeminars in cancer biology2022

AMPK signaling and its targeting in cancer progression and treatment.

Che-Chia Hsu, Danni Peng, Zhen Cai, Hui-Kuan Lin

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 2 pooled it
11.8field-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

163 citing papers in PubMed, 2 syntheses or guidelines pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Organelle contact sites in cancer cells.Cell death & disease · 2026
    Review
  19. Article
  20. Review

103 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

4 authors at 1 institution in 1 country.

Che-Chia HsuDepartment of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC, 27101, USA.
Danni PengDepartment of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC, 27101, USA.
Zhen CaiDepartment of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC, 27101, USA. Electronic address: zcai@wakehealth.edu.
Hui-Kuan LinDepartment of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC, 27101, USA. Electronic address: hulin@wakehealth.edu.
Atrium Health Wake Forest Baptist · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Identification of a new strategy for cancer therapyR01CA193813 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LIN, HUI-KUAN · 2015 to 2019
$1.8M
Novel posttranslational modification in LKB1 activation and cancer developmentR01CA182424 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LIN, HUI-KUAN · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA182424NCI NIH HHS R01 CA193813
6 · The paper itself

Abstract

The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy.

Indexed as

AMP-Activated Protein KinasesNeoplasmsSignal TransductionEnergy MetabolismEpigenesis, GeneticHumansAMP-Activated Protein KinasesAMPKCancerGlucose deprivationMetabolismMitocondriaPhosphorylation

Identifiers

PMID33862221
PMCPMC9768867
OpenAlexW3153431964

What Socratic 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 Socratic graph.