Evidence map›Paper›PMID 18701509›Full record

ArticleCancer research2008

Centrosomal PKCbetaII and pericentrin are critical for human prostate cancer growth and angiogenesis.

Jeewon Kim, Yoon-La Choi, Alice Vallentin, Ben S Hunrichs, Marc K Hellerstein, Donna M Peehl, Daria Mochly-Rosen

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. The E3 ligase Poe promotes Pericentrin degradation.Molecular biology of the cell · 2023
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Promoter Methylation ofInternational journal of molecular sciences · 2021
    Article
  7. Protein Kinase C as a Therapeutic Target in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Classical Protein Kinase C: a novel kinase target in breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Tissue stiffness regulates serine/arginine-rich protein-mediated splicing of the extra domain B-fibronectin isoform in tumors.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Protein kinase C, an elusive therapeutic target?Nature reviews. Drug discovery · 2012
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jeewon KimDepartment of Chemical and Systems Biology, Stanford University, School of Medicine, Stanford, California 94305-5174, USA.
Yoon-La Choi
Alice Vallentin
Ben S Hunrichs
Marc K Hellerstein
Donna M Peehl
Daria Mochly-Rosen
University of California, Berkeley · USSamsung Medical Center · KRStanford University · US

Funding

TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
Hypertrophy, Heart Failure and PKCR01HL076675 · NHLBI · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 2004 to 2008
$1.9M
NCI NIH HHS CA09151NCI NIH HHS T32 CA009151NHLBI NIH HHS R01 HL076675
6 · The paper itself

Abstract

Angiogenesis is critical in the progression of prostate cancer. However, the interplay between the proliferation kinetics of tumor endothelial cells (angiogenesis) and tumor cells has not been investigated. Also, protein kinase C (PKC) regulates various aspects of tumor cell growth, but its role in prostate cancer has not been investigated in detail. Here, we found that the proliferation rates of endothelial and tumor cells oscillate asynchronously during the growth of human prostate cancer xenografts. Furthermore, our analyses suggest that PKCbetaII was activated during increased angiogenesis and that PKCbetaII plays a key role in the proliferation of endothelial cells and tumor cells in human prostate cancer; treatment with a PKCbetaII-selective inhibitor, betaIIV5-3, reduced angiogenesis and tumor cell proliferation. We also find a unique effect of PKCbetaII inhibition on normalizing pericentrin (a protein regulating cytokinesis), especially in endothelial cells as well as in tumor cells. PKCbetaII inhibition reduced the level and mislocalization of pericentrin and normalized microtubule organization in the tumor endothelial cells. Although pericentrin has been known to be up-regulated in epithelial cells of prostate cancers, its level in tumor endothelium has not been studied in detail. We found that pericentrin is up-regulated in human tumor endothelium compared with endothelium adjacent to normal glands in tissues from prostate cancer patients. Our results suggest that a PKCbetaII inhibitor such as betaIIV5-3 may be used to reduce prostate cancer growth by targeting both angiogenesis and tumor cell growth.

Indexed as

Cell ProliferationAdenocarcinomaAnimalsAntigensBlotting, WesternCentrosomeEpithelial CellsFluorescent Antibody TechniqueGas Chromatography-Mass SpectrometryHumansImmunoenzyme TechniquesImmunoprecipitationMaleMiceMice, NudeMicrotubule-Associated ProteinsAntigensMicrotubule-Associated ProteinsPeptide FragmentspericentrinProtein Kinase CProtein Kinase C betaProtein Kinase Inhibitors

Identifiers

PMID18701509
PMCPMC2597632
OpenAlexW2172263810

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.