Evidence map›Paper›PMID 18392133›Full record

ArticleNeoplasia (New York, N.Y.)2008

p21-Activated kinase 1 coordinates aberrant cell survival and pericellular proteolysis in a three-dimensional culture model for premalignant progression of human breast cancer.

Quanwen Li, Stefanie Roshy Mullins, Bonnie F Sloane, Raymond R Mattingly

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  12. In Vitro Models for Studying Invasive Transitions of Ductal Carcinoma In Situ.Journal of mammary gland biology and neoplasia · 2019
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Melatonin: an inhibitor of breast cancer.Endocrine-related cancer · 2015
    Review
  20. Phosphorylation of tyrosine 285 of PAK1 facilitates βPIX/GIT1 binding and adhesion turnover.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article

2 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

4 authors at 2 institutions in 1 country.

Quanwen LiDepartment of Pharmacology and Barbara Ann Karmanos Cancer Institute, Wayne State University, 540 East Canfield Ave, Detroit, MI 48201, USA.
Stefanie Roshy Mullins
Bonnie F Sloane
Raymond R Mattingly
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
CORE 6 : PROJECT LEADERSHIP AND ADMINISTRATIONU54RR020843 · NCRR · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SMITH, JEFFREY W · 2004 to 2009
$19.1M
RESEARCH CORE-- SIGNAL TRANSDUCTIONP30ES006639 · NIEHS · WAYNE STATE UNIVERSITY · PI DERESKI, MARY O · 1994 to 2008
$13.1M
CATHEPSINS IN MALIGNANT PROGRESSION OF MCF 10R01CA056586 · NCI · WAYNE STATE UNIVERSITY · PI SLOANE, BONNIE F · 1992 to 2009
$3.3M
NCI NIH HHS CA22453NCI NIH HHS CA56586NCI NIH HHS P30 CA022453NCI NIH HHS R01 CA056586NCRR NIH HHS U54 RR020843NIEHS NIH HHS P30 ES006639NIEHS NIH HHS P30 ES06639
6 · The paper itself

Abstract

Overexpression of p21-activated kinase 1 (PAK1) occurs during the progression of human breast cancer. We have investigated the role of PAK1 in the premalignant progression of the MCF10 series of human breast epithelial cell lines. Levels of PAK1 expression and activation increased with premalignant progression, and expression of dominant-negative (DN) PAK1 reduced both cell proliferation and migration/invasion. In three-dimensional (3D) overlay cultures in reconstituted basement membrane, the MCF10 series produced an in vitro model for premalignant progression. MCF10AneoT cells formed a hyperplastic morphology in which some spheroids developed abnormal lumens. The MCF10.AT1 line exhibited an atypical hyperplastic morphology of abnormal spheroid clusters that did not form lumens. The MCF10.DCIS cells exhibited dysplastic growth. Expression of DN-PAK1 promoted lumen formation in 3D-cultured MCF10A, NeoT, and AT1 structures, suggesting partial reversion of the premalignant phenotype, but did not affect the atypical budding of AT1 structures or the dysplastic growth of ductal carcinoma in situ structures. Aberrant proteolysis is another important characteristic of breast cancer progression and invasion. DN-PAK1 or knock-down of PAK1 reduced pericellular proteolysis of DQ-collagen IV in the 3D cultures. Treatment of cells with an inhibitor of Rac1 also reduced pericellular proteolysis, and this reduction was reversed by the expression of activated PAK1. Our conclusion is that overexpressed and activated PAK1 may be a key coordinator of aberrant cell survival and proteolysis in breast cancer progression.

Indexed as

Blotting, WesternBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingCell MovementCell ProliferationCells, CulturedCell SurvivalCollagen Type IVDisease ProgressionEpithelial CellsExtracellular MatrixFemaleGenes, DominantHumansImaging, Three-DimensionalModels, BiologicalCollagen Type IVp21-Activated KinasesPAK1 protein, humanPeptide HydrolasesProtease Inhibitors

Identifiers

PMID18392133
PMCPMC2288538
OpenAlexW1565610159

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.