Evidence map›Paper›PMID 9927492›Full record

ArticleThe Journal of clinical investigation1999

p27(kip1) acts as a downstream effector of and is coexpressed with the beta1C integrin in prostatic adenocarcinoma.

M Fornaro, G Tallini, D Q Zheng, W M Flanagan, M Manzotti, L R Languino

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Integrin signaling aberrations in prostate cancer.American journal of translational research · 2009
    Article
  16. Integrins in prostate cancer progression.Endocrine-related cancer · 2008
    Review
  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

6 authors at 3 institutions in 2 countries.

M FornaroDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
G Tallini
D Q Zheng
W M Flanagan
M Manzotti
L R Languino
Yale University · USEuropean Institute of Oncology · ITGilead Sciences (United States) · US

Funding

MOLECULAR REGULATION OF PROSTATE GROWTH BY INTEGRINSR01DK052670 · NIDDK · YALE UNIVERSITY · PI LANGUINO, LUCIA R · 1997 to 2000
$271k
MOLECULAR ANALYSIS OF B1 INTEGRINSR29CA071870 · NCI · YALE UNIVERSITY · PI LANGUINO, LUCIA R · 1996 to 2000
$123k
NCI NIH HHS CA-71870NIDDK NIH HHS DK-52670
6 · The paper itself

Abstract

Integrins are a large family of transmembrane receptors that, in addition to mediating cell adhesion, modulate cell proliferation. The beta1C integrin is an alternatively spliced variant of the beta1 subfamily that contains a unique 48-amino acid sequence in its cytoplasmic domain. We have shown previously that in vitro beta1C inhibits cell proliferation and that in vivo beta1C is expressed in nonproliferative, differentiated epithelium and is selectively downregulated in prostatic adenocarcinoma. Here we show, by immunohistochemistry and immunoblotting analysis, that beta1C is coexpressed in human prostate epithelial cells with the cell-cycle inhibitor p27(kip1), the loss of which correlates with poor prognosis in prostate cancer. In the 37 specimens analyzed, beta1C and p27(kip1) are concurrently expressed in 93% of benign and 84%-91% of tumor prostate cells. Forced expression of beta1C in vitro is accompanied by an increase in p27(kip1) levels, by inhibition of cyclin A-dependent kinase activity, and by increased association of p27(kip1) with cyclin A. beta1C inhibitory effect on cell proliferation is completely prevented by p27(kip1) antisense, but not mismatch oligonucleotides. beta1C expression does not affect either cyclin A or E levels, or cyclin E-associated kinase activity, nor the mitogen-activated protein (MAP) kinase pathway. These findings show a unique mechanism of cell growth inhibition by integrins and point to beta1C as an upstream regulator of p27(kip1) expression and, therefore, a potential target for tumor suppression in prostate cancer.

Indexed as

Cell Cycle ProteinsTumor Suppressor ProteinsAdenocarcinomaCell DivisionCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesDown-RegulationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansIntegrin beta1MaleMicrotubule-Associated ProteinsProstatic NeoplasmsTumor Cells, CulturedCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesIntegrin beta1Microtubule-Associated ProteinsTumor Suppressor Proteins

Identifiers

PMID9927492
PMCPMC407898
OpenAlexW1977093600

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.