Evidence map›Paper›PMID 30242113›Full record

ArticleCancer research2018

CAMKK2 Promotes Prostate Cancer Independently of AMPK via Increased Lipogenesis.

Lucy Penfold, Angela Woods, Phillip Muckett, Alexander Yu Nikitin, Tera R Kent, Shuai Zhang, Rebecca Graham, Alice Pollard, David Carling

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025
    Review
  4. Article
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  9. Article
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  13. Article
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  16. New insights into activation and function of the AMPK.Nature reviews. Molecular cell biology · 2023
    Review
  17. The role of CaMKK2 in Golgi-associated vesicle trafficking.Biochemical Society transactions · 2023
    Review
  18. Article
  19. Article
  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

9 authors at 2 institutions in 2 countries.

Lucy PenfoldMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Angela WoodsMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Phillip MuckettMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Alexander Yu NikitinDepartment of Biomedical Sciences and Cornell Stem Cell Program, Cornell University, Ithaca, New York.ORCID 0000-0002-3729-7982
Tera R KentDepartment of Biomedical Sciences and Cornell Stem Cell Program, Cornell University, Ithaca, New York.
Shuai ZhangMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Rebecca GrahamMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Alice PollardMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom.
David CarlingMRC London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital, London, United Kingdom. dcarling@imperial.ac.uk.
Hammersmith Hospital · GBCornell University · US

Funding

Neuroendocrine mechanisms of prostate cancer progressionR01CA197160 · NCI · CORNELL UNIVERSITY · PI NIKITIN, ALEXANDER Y. · 2015 to 2020
$1.8M
Medical Research Council MC_U120027537MRF_ MRF-023-0001-S-PENFOMRF_ MRF-023-0003-RG-PENFONCI NIH HHS R01 CA197160
6 · The paper itself

Abstract

: New targets are required for treating prostate cancer, particularly castrate-resistant disease. Previous studies reported that calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) expression is increased in human prostate cancer. Here, we show that Camkk2 deletion or pharmacologic inhibition protects against prostate cancer development in a preclinical mouse model that lacks expression of prostate-specific Pten. In contrast, deletion of AMP-activated protein kinase (Ampk) β1 resulted in earlier onset of adenocarcinoma development. These findings suggest for the first time that Camkk2 and Ampk have opposing effects in prostate cancer progression. Loss of CAMKK2

Indexed as

LipogenesisAdenocarcinomaAMP-Activated Protein KinasesAnimalsBenzimidazolesCalcium-Calmodulin-Dependent Protein Kinase KinaseCell CycleCell Line, TumorCell MovementCell ProliferationCell SurvivalCRISPR-Cas SystemsGene DeletionHumansMaleMiceAMP-Activated Protein KinasesAR protein, humanBenzimidazolesCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, humanCamkk2 protein, mouseNaphthalimidesPRKAB1 protein, humanPrkab1 protein, mouseReceptors, AndrogenSTO 609

Identifiers

PMID30242113
PMCPMC6295249
OpenAlexW2891423582

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.