Evidence map›Paper›PMID 37061917›Full record

ArticleCell reports2023

AMPK activation protects against prostate cancer by inducing a catabolic cellular state.

Lucy Penfold, Angela Woods, Alice E Pollard, Julia Arizanova, Eneko Pascual-Navarro, Phillip J Muckett, Marian H Dore, Alex Montoya, Chad Whilding, Louise Fets and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. Metabolic convergence of diabetes and prostate cancer: from dysglycemia to tumor microenvironment reprogramming.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

18 authors at 3 institutions in 2 countries.

Lucy PenfoldMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK. Electronic address: l.penfold12@lms.mrc.ac.uk.
Angela WoodsMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Alice E PollardInstitute of Clinical Sciences, Imperial College London, London, UK.
Julia ArizanovaMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Eneko Pascual-NavarroMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Phillip J MuckettMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Marian H DoreMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Alex MontoyaMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Chad WhildingMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Louise FetsMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Joao MokochinskiMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK.
Theodora A ConstantinImperial Centre for Translational and Experimental Medicine, Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, UK.
Anabel Varela-CarverImperial Centre for Translational and Experimental Medicine, Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, UK.
Damien A LeachImperial Centre for Translational and Experimental Medicine, Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, UK.
Charlotte L BevanImperial Centre for Translational and Experimental Medicine, Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, UK.
Alexander Yu NikitinDepartment of Biomedical Sciences and Cornell Stem Cell Program, Cornell University, Ithaca, NY, USA.
Zoe HallBiomolecular Medicine, Division of Systems Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, UK.
David CarlingMRC London Institute of Medical Sciences, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, UK; Institute of Clinical Sciences, Imperial College London, London, UK. Electronic address: dcarling@imperial.ac.uk.
Hammersmith Hospital · GBImperial College London · GBCornell University · US

Funding

Neuroendocrine mechanisms of prostate cancer progressionR01CA197160 · NCI · CORNELL UNIVERSITY · PI NIKITIN, ALEXANDER Y. · 2015 to 2020
$1.8M
Biotechnology and Biological Sciences Research Council BB/W009633/1Medical Research Council MC-A654-5QB10Medical Research Council MC_U120027537Medical Research Council MC_UP_1605/5NCI NIH HHS R01 CA197160
6 · The paper itself

Abstract

Emerging evidence indicates that metabolic dysregulation drives prostate cancer (PCa) progression and metastasis. AMP-activated protein kinase (AMPK) is a master regulator of metabolism, although its role in PCa remains unclear. Here, we show that genetic and pharmacological activation of AMPK provides a protective effect on PCa progression in vivo. We show that AMPK activation induces PGC1α expression, leading to catabolic metabolic reprogramming of PCa cells. This catabolic state is characterized by increased mitochondrial gene expression, increased fatty acid oxidation, decreased lipogenic potential, decreased cell proliferation, and decreased cell invasiveness. Together, these changes inhibit PCa disease progression. Additionally, we identify a gene network involved in cell cycle regulation that is inhibited by AMPK activation. Strikingly, we show a correlation between this gene network and PGC1α gene expression in human PCa. Taken together, our findings support the use of AMPK activators for clinical treatment of PCa to improve patient outcome.

Indexed as

AMP-Activated Protein KinasesProstatic NeoplasmsHumansLipid MetabolismLipogenesisMalePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAMP-Activated Protein KinasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAMPKcell cycle regulationCP: CancerCP: Metabolismfatty acid oxidationhigh-fat dietlipogenesismetabolismmetastasismitochondriaPGC1αprostate cancer

Identifiers

PMID37061917
PMCPMC10576838
OpenAlexW4365813120

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.