Evidence map›Paper›PMID 18202186›Full record

ArticleThe American journal of pathology2008

Regulation of Cripto-1 signaling and biological activity by caveolin-1 in mammary epithelial cells.

Caterina Bianco, Luigi Strizzi, Mario Mancino, Kazuhide Watanabe, Monica Gonzales, Shin Hamada, Ahmed Raafat, Lawson Sahlah, Cindy Chang, Federica Sotgia and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. From embryonic development to human diseases: The functional role of caveolae/caveolin.Birth defects research. Part C, Embryo today : reviews · 2016
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Targeting the embryonic gene Cripto-1 in cancer and beyond.Expert opinion on therapeutic patents · 2010
    Review
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

13 authors at 4 institutions in 2 countries.

Caterina BiancoNational Cancer Institute, Bethesda, MD 20892, USA.
Luigi Strizzi
Mario Mancino
Kazuhide Watanabe
Monica Gonzales
Shin Hamada
Ahmed Raafat
Lawson Sahlah
Cindy Chang
Federica Sotgia
Nicola Normanno
Michael Lisanti
David S Salomon
National Institutes of Health · USThomas Jefferson University · USIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITRutgers, The State University of New Jersey · US

Funding

Texas Tech Center for Translational Research and Rural Health - Research Capacity CoreU54MD020892 · NIMHD · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI Lance R. McMahon, Naima Moustaid-Moussa · 2026 to 2026
$10.0M
The Role of Cripto in the Pathogenesis of Breast and Colon CancerZIABC009003 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SALOMON, DAVID · 2009 to 2016
$9.4M
THE ROLE OF EGF-RELATED PEPTIDES IN THE PATHOGENESIS OF BREAST AND COLON CANCERZ01BC009003 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SALOMON, DAVID · 1996 to 2008
$2.4M
Intramural NIH HHSNIMHD NIH HHS U54 MD020892
6 · The paper itself

Abstract

Human and mouse Cripto-1 (CR-1/Cr-1) proteins play an important role in mammary gland development and tumorigenesis. In this study, we examined the relationship between Cripto-1 and caveolin-1 (Cav-1), a membrane protein that acts as a tumor suppressor in the mammary gland. Cripto-1 was found to interact with Cav-1 in COS7 cells and mammary epithelial cells. Using EpH4 mouse mammary epithelial cells expressing Cr-1 (EpH4 Cr-1) or Cr-1 and Cav-1 (EpH4 Cr-1/Cav-1), we demonstrate that Cav-1 expression markedly reduced the ability of Cr-1 to enhance migration, invasion, and formation of branching structures in EpH4 Cr-1/Cav-1 cells as compared to EpH4 Cr-1 cells. Furthermore, coexpression of Cav-1 together with Cr-1 in EpH4 Cr-1/Cav-1 cells inhibited Cr-1-mediated activation of c-src and mitogen-activated protein kinase signaling pathways. Conversely, primary mammary epithelial cells isolated from Cav-1 null(-/-)/mouse mammary tumor virus-CR-1 transgenic animals showed enhanced motility and activation of mitogen-activated protein kinase and c-src as compared to Cav-1(+/-)/CR-1 mammary cells. Finally, mammary tumors derived from mouse mammary tumor virus-CR-1 mice showed a dramatic reduction of Cav-1 expression as compared to mammary tissue from normal FVB/N mice, suggesting that in vivo Cav-1 is down-regulated during the process of CR-1-mediated mammary tumorigenesis.

Indexed as

AnimalsBlotting, WesternCaveolin 1Cell MovementChlorocebus aethiopsCOS CellsCSK Tyrosine-Protein KinaseEnzyme ActivationEpidermal Growth FactorEpithelial CellsExtracellular Signal-Regulated MAP KinasesFemaleFluorescent Antibody TechniqueHumansImmunoprecipitationMammary Glands, AnimalCaveolin 1CSK protein, humanCSK Tyrosine-Protein KinaseEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesMembrane GlycoproteinsNeoplasm ProteinsProtein-Tyrosine Kinasessrc-Family KinasesTdgf1 protein, mouse

Identifiers

PMID18202186
PMCPMC2312365
OpenAlexW2001670625

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.