Evidence map›Paper›PMID 16314838›Full record

ArticleOncogene2006

RhoC GTPase is required for PC-3 prostate cancer cell invasion but not motility.

H Yao, E J Dashner, C M van Golen, K L van Golen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Role of the lncRNA ABHD11-ASMolecular cancer · 2017
    Article
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  15. Article
  16. Review
  17. RhoC GTPase activation assay.Journal of visualized experiments : JoVE · 2010
    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

4 authors at 1 institution in 1 country.

H YaoDivision of Hematology/Oncology, The Department of Internal Medicine, The University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109-0548, USA.
E J Dashner
C M van Golen
K L van Golen
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
VACCINIA PSA FOR ANDROGEN-MODULATED POST-SURGICAL RECURRENCE OF PROSTATE CANCERP50CA069568 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COONEY, KATHLEEN A · 1995 to 2013
$31.3M
NCI NIH HHS 5 P30 CA46592NCI NIH HHS P50 CA69568
6 · The paper itself

Abstract

It is projected that in 2005, approximately 220 900 men will be newly diagnosed with carcinoma of the prostate (CaP). Men who are diagnosed with locally advanced or metastatic disease undergo androgen ablation therapy and most will relapse and progress within 18 months. Metastasis to bone is the major clinical concern during CaP progression, as it is associated with intractable pain, bone fracture and paralysis resulting from spinal cord compression. Therefore, an understanding of the key mechanisms involved in CaP cell bone metastasis is vital to development of novel treatments. The Rho GTPases are molecular switches involved in cell survival, motility and invasion. Increased expression of RhoC GTPase is linked to enhanced metastatic potential in multiple cancers; however, the role of RhoC GTPase in CaP metastasis has not been addressed. In the current study, we demonstrate that RhoC GTPase is expressed and active in PC-3 CaP cells. RhoC inhibition, either pharmacologically with C3 exotransferase or molecularly through expression of a dominant-negative RhoC, promotes IGF-I stimulated random motility but decreases in vitro invasion and experimental metastases. Inhibition of RhoC activity results in drastic morphologic changes and alterations in the expression and distribution of focal adhesion-related proteins. These data suggest that RhoC inhibition leads to activation of other GTPases involved in nondirected motility and that expression of active RhoC is required for the invasive phenotype of PC-3 cells.

Indexed as

ActinsADP Ribose TransferasesBotulinum Toxinscdc42 GTP-Binding ProteinCell Line, TumorCell MovementFocal Adhesion Protein-Tyrosine KinasesGTPase-Activating ProteinsHumansInsulin-Like Growth Factor IMaleNeoplasm InvasivenessProstatic Neoplasmsrac1 GTP-Binding ProteinrhoC GTP-Binding Proteinrho GTP-Binding ProteinsActinsADP Ribose TransferasesBotulinum Toxinscdc42 GTP-Binding Proteinexoenzyme C3, Clostridium botulinumFocal Adhesion Protein-Tyrosine KinasesGIT2 protein, humanGTPase-Activating ProteinsInsulin-Like Growth Factor Irac1 GTP-Binding ProteinrhoC GTP-Binding ProteinRHOC protein, humanrho GTP-Binding ProteinsVinculin

Identifiers

PMID16314838
OpenAlexW2077893826

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.