Evidence map›Paper›PMID 24129850›Full record

ArticleJournal of cellular physiology2014

The interplay of AMP-activated protein kinase and androgen receptor in prostate cancer cells.

Min Shen, Zhen Zhang, Manohar Ratnam, Q Ping Dou

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  11. Urolithin B, a newly identified regulator of skeletal muscle mass.Journal of cachexia, sarcopenia and muscle · 2017
    Article
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  17. Berberine, an epiphany against cancer.Molecules (Basel, Switzerland) · 2014
    Review
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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 2 institutions in 1 country.

Min ShenDepartment of Pharmacology, School of Medicine, Wayne State University, Detroit, Michigan; Barbara Ann Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan.
Zhen Zhang
Manohar Ratnam
Q Ping Dou
The Barbara Ann Karmanos Cancer Institute · USWayne State University · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI Jennifer L Beebe-Dimmer · 1985 to 2026
$68.4M
Roles of polymorphic COMT, tea polyphenols and proteasome in cancer preventionR01CA120009 · NCI · WAYNE STATE UNIVERSITY · PI DOU, QING PING · 2006 to 2010
$1.5M
The BCA2 Ubiquitin E3 Ligase as a Target in Breast CancerR01CA127258 · NCI · WAYNE STATE UNIVERSITY · PI DOU, QING PING · 2007 to 2011
$1.2M
(PQA1) Regulation of Metformin Response by Breast Cancer Associated Gene 2 (BCA2)R21CA184788 · NCI · WAYNE STATE UNIVERSITY · PI DOU, QING PING · 2014 to 2015
$364k
NCI NIH HHS 1R01CA20009NCI NIH HHS 3R01CA120009-04S1NCI NIH HHS 5R01CA127258-05NCI NIH HHS P30 CA022453NCI NIH HHS (P30 CA22453NCI NIH HHS R01 CA120009NCI NIH HHS R01 CA127258NCI NIH HHS R21 CA184788
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) has recently emerged as a potential target for cancer therapy due to the observation that activation of AMPK inhibits tumor cell growth. It is well-known that androgen receptor (AR) signaling is a major driver for the development and progression of prostate cancer and that downregulation of AR is a critical step in the induction of apoptosis in prostate cancer cells. However, little is known about the potential interaction between AMPK and AR signaling pathways. In the current study, we showed that activation of AMPK by metformin caused decrease of AR protein level through suppression of AR mRNA expression and promotion of AR protein degradation, demonstrating that AMPK activation is upstream of AR downregulation. We also showed that inhibition of AR function by an anti-androgen or its siRNA enhanced AMPK activation and growth inhibition whereas overexpression of AR delayed AMPK activation and increased prostate cancer cellular resistance to metformin treatment, suggesting that AR suppresses AMPK signaling-mediated growth inhibition in a feedback mechanism. Our findings thus reveal a novel AMPK-AR regulatory loop in prostate cancer cells and should have a potential clinical significance.

Indexed as

AMP-Activated Protein KinasesAnilidesAntineoplastic AgentsCell Line, TumorDose-Response Relationship, DrugGene Expression Regulation, NeoplasticHumansMaleMetforminNitrilesProstatic NeoplasmsReceptors, AndrogenSignal TransductionTosyl CompoundsAMP-Activated Protein KinasesAnilidesAntineoplastic AgentsbicalutamideMetforminNitrilesReceptors, AndrogenTosyl Compounds

Identifiers

PMID24129850
PMCPMC3947449
OpenAlexW2165662050

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.