Evidence map›Paper›PMID 22955280›Full record

ArticleThe Journal of biological chemistry2012

Activation of nuclear factor κB (NF-κB) in prostate cancer is mediated by protein kinase C epsilon (PKCepsilon).

Rachana Garg, Jorge Blando, Carlos J Perez, HongBin Wang, Fernando J Benavides, Marcelo G Kazanietz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Chemopreventive Activity of Ellagitannins fromPlants (Basel, Switzerland) · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Urobiome: An outlook on the metagenome of urological diseases.Investigative and clinical urology · 2021
    Review
  16. TRIM47 activates NF-κB signaling via PKC-ε/PKD3 stabilization and contributes to endocrine therapy resistance in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 4 institutions in 1 country.

Rachana GargDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Jorge Blando
Carlos J Perez
HongBin Wang
Fernando J Benavides
Marcelo G Kazanietz
University of Pennsylvania · USGenesis Foundation · USThe University of Texas at Austin · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Prostate Carcinogensis and PKC SignalingR01CA089202 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KAZANIETZ, MARCELO G. · 2001 to 2015
$4.5M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA089202NCI NIH HHS R01-CA89202
6 · The paper itself

Abstract

Protein kinase C ε (PKCε) has emerged as an oncogenic kinase and plays important roles in cell survival, mitogenesis and invasion. PKCε is up-regulated in most epithelial cancers, including prostate, breast, and lung cancer. Here we report that PKCε is an essential mediator of NF-κB activation in prostate cancer cells. A strong correlation exists between PKCε overexpression and NF-κB activation status in prostate cancer cells. Moreover, transgenic overexpression of PKCε in the mouse prostate causes preneoplastic lesions that display significant NF-κB hyperactivation. PKCε RNAi depletion or inhibition in prostate cancer cells diminishes NF-κB translocation to the nucleus with subsequent impairment of both activation of NF-κB transcription and induction of NF-κB responsive genes in response to the proinflammatory cytokine tumor necrosis factor α (TNFα). On the other hand, PKCε overexpression in normal prostate cells enhances activation of the NF-κB pathway. A mechanistic analysis revealed that TNFα activates PKCε via a C1 domain/diacylglycerol-dependent mechanism that involves phosphatidylcholine-phospholipase C. Moreover, PKCε facilitates the assembly of the TNF receptor-I signaling complex to trigger NF-κB activation. Our studies identified a molecular link between PKCε and NF-κB that controls key responses implicated in prostate cancer progression.

Indexed as

Signal TransductionActive Transport, Cell NucleusAnimalsCell Line, TumorGene Expression Regulation, NeoplasticGenes, ReporterHumansI-kappa B ProteinsLuciferases, RenillaMaleMiceMice, TransgenicNF-kappa BNF-KappaB Inhibitor alphaProstatic NeoplasmsProtein BindingI-kappa B ProteinsLuciferases, RenillaNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mousephosphatidylcholine-specific phospholipase CProtein Kinase C-epsilonReceptors, Tumor Necrosis Factor, Type IRELA protein, humanTranscription Factor RelATumor Necrosis Factor-alphaType C Phospholipases

Identifiers

PMID22955280
PMCPMC3481351
OpenAlexW2011397271

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.