Evidence map›Paper›PMID 19855435›Full record

ArticleOncogene2010

Overexpression of myosin VI in prostate cancer cells enhances PSA and VEGF secretion, but has no effect on endocytosis.

C Puri, M V Chibalina, S D Arden, A J Kruppa, J Kendrick-Jones, F Buss

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Lemur Tyrosine Kinases and Prostate Cancer: A Literature Review.International journal of molecular sciences · 2021
    Review
  9. Diverse functions of myosin VI in spermiogenesis.Histochemistry and cell biology · 2021
    Review
  10. Article
  11. Shear Stress Increases V-HCellular and molecular bioengineering · 2020
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Myosin VI contributes to malignant proliferation of human glioma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    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 2 institutions in 1 country.

C PuriCambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Cambridge, UK.
M V Chibalina
S D Arden
A J Kruppa
J Kendrick-Jones
F Buss
University of Cambridge · GBMRC Laboratory of Molecular Biology · GB

Funding

Cancer Research UK A7548Medical Research Council MC_U105184323Wellcome Trust
6 · The paper itself

Abstract

Tissue expression microarrays, employed to determine the players and mechanisms leading to prostate cancer development, have consistently shown that myosin VI, a unique actin-based motor, is upregulated in medium-grade human prostate cancers. Thus, to understand the role of myosin VI in prostate cancer development, we have characterized its intracellular localization and function in the prostate cancer cell line LNCaP. Using light and electron microscopy, we identified myosin VI on Rab5-positive early endosomes, as well as on recycling endosomes and the trans-Golgi network. Intracellular targeting seems to involve two myosin VI-interacting proteins, GIPC and LMTK2, both of which can be co-immunoprecipitated with myosin VI from LNCaP cells. The absence of Disabled-2 (Dab2), a tumour suppressor and myosin VI-binding partner, inhibits recruitment of myosin VI to endocytic structures at the plasma membrane in LNCaP cells, but interestingly has no effect on endocytosis. Small interfering RNA-mediated downregulation of myosin VI expression results in a significant reduction in prostate-specific antigen (PSA) and vascular endothelial growth factor (VEGF) secretion in LNCaP cells. Our results suggest that in prostate cancer cells, myosin VI regulates protein secretion, but the overexpression of myosin VI has no major impact on clathrin-mediated endocytosis.

Indexed as

EndocytosisAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBlotting, WesternCell LineCell Line, TumorEndosomesGene ExpressionGolgi ApparatusGreen Fluorescent ProteinsHeLa CellsHumansMaleMembrane ProteinsMicroscopy, FluorescenceMicroscopy, ImmunoelectronAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDAB2 protein, humanGIPC1 protein, humanGreen Fluorescent ProteinsLMTK2 protein, humanMembrane ProteinsMyosin Heavy Chainsmyosin VIProstate-Specific AntigenProtein Serine-Threonine KinasesRecombinant Fusion ProteinsTumor Suppressor ProteinsVascular Endothelial Growth Factor A

Identifiers

PMID19855435
PMCPMC2871299
OpenAlexW1992590802

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.