Evidence map›Paper›PMID 18927239›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

A dual role for oncostatin M signaling in the differentiation and death of mammary epithelial cells in vivo.

Paul G Tiffen, Nader Omidvar, Nuria Marquez-Almuina, Dawn Croston, Christine J Watson, Richard W E Clarkson

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

44 citing papers in PubMed, 69 citations in OpenAlex.

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  15. The cJUN NHCell death and differentiation · 2018
    Article
  16. ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  17. Review
  18. Article
  19. Molecular biology of the cell · 2018
    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.

Paul G TiffenDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Nader Omidvar
Nuria Marquez-Almuina
Dawn Croston
Christine J Watson
Richard W E Clarkson
Cardiff University · GBUniversity of Cambridge · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Recent studies in breast cancer cell lines have shown that oncostatin M (OSM) not only inhibits proliferation but also promotes cell detachment and enhances cell motility. In this study, we have looked at the role of OSM signaling in nontransformed mouse mammary epithelial cells in vitro using the KIM-2 mammary epithelial cell line and in vivo using OSM receptor (OSMR)-deficient mice. OSM and its receptor were up-regulated approximately 2 d after the onset of postlactational mammary regression, in response to leukemia inhibitory factor (LIF)-induced signal transducer and activator of transcription-3 (STAT3). This resulted in sustained STAT3 activity, increased epithelial apoptosis, and enhanced clearance of epithelial structures during the remodeling phase of mammary involution. Concurrently, OSM signaling precipitated the dephosphorylation of STAT5 and repressed expression of the milk protein genes beta-casein and whey acidic protein (WAP). Similarly, during pregnancy, OSM signaling suppressed beta-casein and WAP gene expression. In vitro, OSM but not LIF persistently down-regulated phosphorylated (p)-STAT5, even in the continued presence of prolactin. OSM also promoted the expression of metalloproteinases MMP3, MMP12, and MMP14, which, in vitro, were responsible for OSM-specific apoptosis. Thus, the sequential activation of IL-6-related cytokines during mammary involution culminates in an OSM-dependent repression of epithelial-specific gene expression and the potentiation of epithelial cell extinction mediated, at least in part, by the reciprocal regulation of p-STAT5 and p-STAT3.

Indexed as

AnimalsApoptosisCell DeathCell DifferentiationCells, CulturedEpithelial CellsFemaleGene Expression RegulationLactationMammary Glands, AnimalMiceMice, KnockoutMilkMitogen-Activated Protein Kinase 3Oncostatin MOncostatin M Receptor beta SubunitMitogen-Activated Protein Kinase 3Oncostatin MOncostatin M Receptor beta SubunitOsmr protein, mouseStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID18927239
PMCPMC5419408
OpenAlexW1984345184

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.