Evidence map›Paper›PMID 23550155›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

c-Myc phosphorylation by PKCζ represses prostate tumorigenesis.

Ji Young Kim, Tania Valencia, Shadi Abu-Baker, Juan Linares, Sang Jun Lee, Tomoko Yajima, Jing Chen, Alexey Eroshkin, Elias A Castilla, Laurence M Brill and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

  1. PMA exerts anti-leukemia effect in PhCancer cell international · 2025
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  18. Protein kinase C as a tumor suppressor.Seminars in cancer biology · 2018
    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

14 authors at 3 institutions in 2 countries.

Ji Young KimSanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.
Tania Valencia
Shadi Abu-Baker
Juan Linares
Sang Jun Lee
Tomoko Yajima
Jing Chen
Alexey Eroshkin
Elias A Castilla
Laurence M Brill
Mario Medvedovic
Michael Leitges
Jorge Moscat
Maria T Diaz-Meco
Sanford Burnham Prebys Medical Discovery Institute · USUniversity of Cincinnati Medical Center · USUniversity of Oslo · NO

Funding

Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
The p62/atypical PKC signaling complex in Th2 differentiation and asthmaR01AI072581 · NIAID · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2008 to 2012
$2.1M
Role and mechanism of action of p62/Sqstm1 in Ras-induced tumorigenesis in lungR01CA132847 · NCI · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2009 to 2013
$2.0M
The Par-4/PKCz complex in prostate cancerR01CA134530 · NCI · UNIVERSITY OF CINCINNATI · PI DIAZ MECO CONDE, MARIA TERESA · 2009 to 2013
$1.8M
Obesity-Induced Inflammation and Insulin Resistance by the p62/PKCzeta SignalingR01DK088107 · NIDDK · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2010 to 2012
$1.1M
NCATS NIH HHS UL1 TR000077NCI NIH HHS PC080441NCI NIH HHS R01 CA132847NCI NIH HHS R01CA132847NCI NIH HHS R01 CA134530NCI NIH HHS R01CA134530NIAID NIH HHS R01 AI072581NIAID NIH HHS R01AI072581NIDDK NIH HHS R01 DK088107NIDDK NIH HHS R01DK088107
6 · The paper itself

Abstract

Studies showing reduced PKCζ expression or enzymatic activity in different types of human cancers support the clinical relevance of PKCζ as a tumor suppressor. However, the in vivo role of PKCζ and its mechanisms of action in prostate cancer remain unclear. Here we demonstrate that the genetic inactivation of PKCζ in mice results in invasive prostate carcinoma in vivo in the context of phosphatase and tensin homolog deficiency. Bioinformatic analysis of human prostate cancer gene-expression sets revealed increased c-Myc transcriptional activity in PKCζ-inactive cells, which correlated with increased cell growth, invasion, and metastasis. Interestingly, PKCζ knockdown or the overexpression of a kinase-inactive mutant resulted in enhanced cell proliferation and invasion in vitro through increased c-Myc mRNA and protein levels and decreased Ser-373 phosphorylation of c-Myc. Analysis of prostate cancer samples demonstrated increased expression and decreased phosphorylation of c-Myc at Ser-373 in PKCζ knockout tumors. In vivo xenograft studies revealed that c-Myc phosphorylation by PKCζ is a critical event in the control of metastasis. Collectively, these results establish PKCζ as an important tumor suppressor and regulator of c-Myc function in prostate cancer.

Indexed as

AnimalsBlotting, WesternCell Transformation, NeoplasticComputational BiologyGene Expression Regulation, NeoplasticLuciferasesMaleMiceMicroarray AnalysisNeoplasm MetastasisPhosphorylationProstatic NeoplasmsProtein Kinase CProtein Kinase C zetaProto-Oncogene Proteins c-mycPTEN PhosphohydrolaseLuciferasesMyc protein, mouseProtein Kinase CProtein Kinase C zetaProto-Oncogene Proteins c-mycPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID23550155
PMCPMC3631641
OpenAlexW2050852507

What OpenQuestion holds

Textmetadata
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.