Evidence map›Paper›PMID 9777939›Full record

ArticleThe American journal of pathology1998

Beta1C integrin in epithelial cells correlates with a nonproliferative phenotype: forced expression of beta1C inhibits prostate epithelial cell proliferation.

M Fornaro, M Manzotti, G Tallini, A E Slear, S Bosari, E Ruoslahti, L R Languino

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Analysis of conserved residues in the betapat-3 cytoplasmic tail reveals important functions of integrin in multiple tissues.Developmental dynamics : an official publication of the American Association of Anatomists · 2010
    Article
  6. Article
  7. Article
  8. Integrin signaling aberrations in prostate cancer.American journal of translational research · 2009
    Article
  9. Integrins in prostate cancer progression.Endocrine-related cancer · 2008
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 3 institutions in 2 countries.

M FornaroDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
M Manzotti
G Tallini
A E Slear
S Bosari
E Ruoslahti
L R Languino
Yale University · USCancer Research Center · USEuropean Institute of Oncology · IT

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

The expression of the beta1C integrin, an alternatively spliced variant of the beta1 subunit, was investigated in human adult and fetal tissues. In the adult, beta1C immunoreactivity was found in nonproliferative, differentiated simple, and/or pseudostratified epithelia in prostate glands and liver bile ducts. In contrast, beta1C was undetectable in stratified squamous epithelium of the epidermis and/or in hepatocytes. Luminal prostate epithelial cells expressed beta1C in vivo and in vitro, but no beta1C was seen in basal cells, which are proliferating cells. Fetal prostate expressed beta1C in differentiated glands that had a defined lumen, but not in budding glands, indicating that beta1C is a marker of prostate epithelium differentiation. The beta1C and the common beta1A variants are differentially distributed: beta1A was found in luminal and basal epithelial as well as in stromal cells in the prostate. In the liver, beta1C and beta1A were coexpressed in biliary epithelium, whereas vascular cells expressed only beta1A. Because we found beta1C in nonproliferative and differentiated epithelium, we investigated whether beta1C could have a causal role in inhibiting epithelial cell proliferation. The results showed that exogenous expression of a beta1C, but not of a beta1A, cytoplasmic domain chimeric construct, completely inhibited thymidine incorporation in response to serum by prostate cancer epithelial cells. Consistent with these in vitro results, beta1C appeared to be downregulated in prostate glands that exhibit regenerative features in benign hyperplastic epithelium. These data show that the presence of beta1C integrins in epithelial cells correlates with a nonproliferative, differentiated phenotype and is growth inhibitory to prostate epithelial cells in vitro. These findings indicate a novel pathophysiological role for this integrin variant in epithelial cell proliferation.

Indexed as

Alternative SplicingBile DuctsCell DivisionEmbryonic and Fetal DevelopmentEpithelial CellsHumansImmunoenzyme TechniquesIntegrin beta1KeratinsLiverMalePhenotypeProstateProstatic HyperplasiaProstatic NeoplasmsRegenerationIntegrin beta1KeratinsThymidine

Identifiers

PMID9777939
PMCPMC1853035
OpenAlexW1753444805

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.