Evidence map›Paper›PMID 19228372›Full record

ReviewMolecular cancer2009

Protein kinase C epsilon: an oncogene and emerging tumor biomarker.

Michael A Gorin, Quintin Pan

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Article
  3. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Variants in PRKCE and KLC1, Potential Regulators of Type I Psoriasis.Clinical, cosmetic and investigational dermatology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. A bismuth diethyldithiocarbamate compound induced apoptosis via mitochondria-dependent pathway and suppressed invasion in MCF-7 breast cancer cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
    Article
  18. Article
  19. Regulation of Autophagy by Protein Kinase C-ε in Breast Cancer Cells.International journal of molecular sciences · 2020
    Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Michael A GorinUniversity of Miami, Miller School of Medicine, Miami, FL 33136, USA. magorin@med.miami.edu
Quintin Pan
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USUniversity of Miami · US

Funding

Therapeutic Potential and Mechanism of Action of Potent Small Molecule InhibitorsP50CA097248 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WOLF, GREGORY T · 2002 to 2013
$25.3M
Role of PKCepsilon in Oral CancerR01CA135096 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PAN, QUINTIN · 2008 to 2012
$1.8M
NCI NIH HHS P50 CA097248NCI NIH HHS P50-CA097248NCI NIH HHS R01 CA135096NCI NIH HHS R01-CA135096
6 · The paper itself

Abstract

Members of the protein kinase C (PKC) family have long been studied for their contributions to oncogenesis. Among the ten different isoforms of this family of serine/threonine kinases, protein kinase C epsilon (PKC epsilon) is one of the best understood for its role as a transforming oncogene. In vitro, overexpression of PKC epsilon has been demonstrated to increase proliferation, motility, and invasion of fibroblasts or immortalized epithelial cells. In addition, xenograft and transgenic animal models have clearly shown that overexpression of PKC epsilon is tumorigenic resulting in metastatic disease. Perhaps most important in implicating the epsilon isoform in oncogenesis, PKC epsilon has been found to be overexpressed in tumor-derived cell lines and histopathological tumor specimens from various organ sites. Combined, this body of work provides substantial evidence implicating PKC epsilon as a transforming oncogene that plays a crucial role in establishing an aggressive metastatic phenotype. Reviewed here is the literature that has led to the current understanding of PKC epsilon as an oncogene. Moreover, this review focuses on the PKC epsilon-mediated signaling network for cell motility and explores the interaction of PKC epsilon with three major PKC epsilon signaling nodes: RhoA/C, STAT3 and Akt. Lastly, the emerging role of PKC epsilon as a tumor biomarker is discussed.

Indexed as

AnimalsBiomarkers, TumorHumansNeoplasm MetastasisProtein BindingProtein Kinase C-epsilonSignal TransductionBiomarkers, TumorProtein Kinase C-epsilon

Identifiers

PMID19228372
PMCPMC2647895
OpenAlexW2161407210

What OpenQuestion 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 OpenQuestion graph.