Evidence map›Paper›PMID 20876802›Full record

ArticleCancer research2010

RasGRP3 contributes to formation and maintenance of the prostate cancer phenotype.

Dazhi Yang, Noemi Kedei, Luowei Li, Juan Tao, Julia F Velasquez, Aleksandra M Michalowski, Balázs I Tóth, Rita Marincsák, Attila Varga, Tamás Bíró and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Regulation of the Small GTPase Ras and Its Relevance to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Gene polymorphisms and oral cancer risk in tobacco habitués.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. 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

12 authors at 3 institutions in 2 countries.

Dazhi YangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4255 , USA.
Noemi Kedei
Luowei Li
Juan Tao
Julia F Velasquez
Aleksandra M Michalowski
Balázs I Tóth
Rita Marincsák
Attila Varga
Tamás Bíró
Stuart H Yuspa
Peter M Blumberg
National Cancer Institute · USCenter for Cancer Research · USUniversity of Debrecen · HU

Funding

Molecular Mechanism of Action of Phorbol EsterZIABC005270 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BLUMBERG, PETER · 2009 to 2018
$18.4M
Pathways that Suppress or Accelerate Premalignant Progression of Squamous CancerZIABC005445 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YUSPA, STUART H. · 2009 to 2022
$15.7M
MOLECULAR MECHANISM OF ACTION OF PHORBOL ESTER TUMOR PROMOTERSZ01BC005270 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BLUMBERG, PETER · 1996 to 2008
$4.3M
Intramural NIH HHS Z01 BC005270Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC005270
6 · The paper itself

Abstract

RasGRP3 mediates the activation of the Ras signaling pathway that is present in many human cancers. Here, we explored the involvement of RasGRP3 in the formation and maintenance of the prostate cancer phenotype. RasGRP3 expression was elevated in multiple human prostate tumor tissue samples and in the human androgen-independent prostate cancer cell lines PC-3 and DU 145 compared with the androgen-dependent prostate cancer cell line LNCaP. Downregulation of endogenous RasGRP3 in PC-3 and DU 145 cells reduced Ras-GTP formation, inhibited cell proliferation, impeded cell migration, and induced apoptosis. Anchorage-independent growth of the PC-3 cells and tumor formation in mouse xenografts of both cell lines were likewise inhibited. Inhibition of RasGRP3 expression reduced AKT and extracellular signal-regulated kinase 1/2 phosphorylation and sensitized the cells to killing by carboplatin. Conversely, exogenous RasGRP3 elevated Ras-GTP, stimulated proliferation, and provided resistance to phorbol 12-myristate 13-acetate-induced apoptosis in LNCaP cells. RasGRP3-overexpressing LNCaP cells displayed a markedly enhanced rate of xenograft tumor formation in both male and female mice compared with the parental line. Suppression of RasGRP3 expression in these cells inhibited downstream RasGRP3 responses, caused the cells to resume the LNCaP morphology, and suppressed growth, confirming the functional role of RasGRP3 in the altered behavior of these cells. We conclude that RasGRP3 contributes to the malignant phenotype of the prostate cancer cells and may constitute a novel therapeutic target for human prostate cancer.

Indexed as

Cell DivisionCell Line, TumorDown-RegulationGene Expression Regulation, NeoplasticGuanine Nucleotide Exchange FactorsHumansMalePhenotypeProstatic Neoplasmsras Guanine Nucleotide Exchange FactorsReverse Transcriptase Polymerase Chain ReactionRNA, NeoplasmGuanine Nucleotide Exchange FactorsRASGRP3 protein, humanras Guanine Nucleotide Exchange FactorsRNA, Neoplasm

Identifiers

PMID20876802
PMCPMC2955810
OpenAlexW2022110987

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.