Evidence map›Paper›PMID 25077702›Full record

ArticleNeoplasia (New York, N.Y.)2014

The balance of cell surface and soluble type III TGF-β receptor regulates BMP signaling in normal and cancerous mammary epithelial cells.

Catherine E Gatza, Jennifer L Elderbroom, Sun Young Oh, Mark D Starr, Andrew B Nixon, Gerard C Blobe

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review
  8. A tumor-promoting role for soluble TβRIII in glioblastoma.Molecular and cellular biochemistry · 2021
    Article
  9. Observational
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. N-cadherin mediates the migration of MCF-10A cells undergoing bone morphogenetic protein 4-mediated epithelial mesenchymal transition.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  17. 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 1 institution in 1 country.

Catherine E GatzaDepartment of Medicine, Duke University Medical Center, Durham, NC.
Jennifer L ElderbroomDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC.
Sun Young OhDepartment of Medicine, Duke University Medical Center, Durham, NC.
Mark D StarrDepartment of Medicine, Duke University Medical Center, Durham, NC.
Andrew B NixonDepartment of Medicine, Duke University Medical Center, Durham, NC.
Gerard C BlobeDepartment of Medicine, Duke University Medical Center, Durham, NC; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC. Electronic address: gerard.blobe@duke.edu.
Duke Medical Center · US

Funding

Function of TbRIII as a BMP Co-receptor in Human CancerR01CA136786 · NCI · DUKE UNIVERSITY · PI BLOBE, GERARD C · 2009 to 2013
$1.8M
Elucidating the Role of the TGF-Beta Receptor III in Breast CarcinogenesisF32CA136125 · NCI · DUKE UNIVERSITY · PI GATZA, CATHERINE · 2008 to 2011
$150k
NCI NIH HHS BC093966NCI NIH HHS F32 CA136125NCI NIH HHS F32CA136125NCI NIH HHS R01 CA136786NCI NIH HHS R01-CA136786
6 · The paper itself

Abstract

Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily that are over-expressed in breast cancer, with context dependent effects on breast cancer pathogenesis. The type III TGF-β receptor (TβRIII) mediates BMP signaling. While TβRIII expression is lost during breast cancer progression, the role of TβRIII in regulating BMP signaling in normal mammary epithelium and breast cancer cells has not been examined. Restoring TβRIII expression in a 4T1 murine syngeneic model of breast cancer suppressed Smad1/5/8 phosphorylation and inhibited the expression of the BMP transcriptional targets, Id1 and Smad6, in vivo. Similarly, restoring TβRIII expression in human breast cancer cell lines or treatment with sTβRIII inhibited BMP-induced Smad1/5/8 phosphorylation and BMP-stimulated migration and invasion. In normal mammary epithelial cells, shRNA-mediated silencing of TβRIII, TβRIII over-expression, or treatment with sTβRIII inhibited BMP-mediated phosphorylation of Smad1/5/8 and BMP induced migration. Inhibition of TβRIII shedding through treatment with TAPI-2 or expression of a non-shedding TβRIII mutant rescued TβRIII mediated inhibition of BMP induced Smad1/5/8 phosphorylation and BMP induced migration and/or invasion in both in normal mammary epithelial cells and breast cancer cells. Conversely, expression of a TβRIII mutant, which exhibited increased shedding, significantly reduced BMP-mediated Smad1/5/8 phosphorylation, migration, and invasion. These data demonstrate that TβRIII regulates BMP-mediated signaling and biological effects, primarily through the ligand sequestration effects of sTβRIII in normal and cancerous mammary epithelial cells and suggest that the ratio of membrane bound versus sTβRIII plays an important role in mediating these effects.

Indexed as

Signal TransductionAnimalsBone Morphogenetic ProteinsBreast NeoplasmsCell Line, TumorCell MovementDisease Models, AnimalEpithelial CellsFemaleHumansMiceMutationProteoglycansReceptors, Transforming Growth Factor betabetaglycanBone Morphogenetic ProteinsProteoglycansReceptors, Transforming Growth Factor beta

Identifiers

PMID25077702
PMCPMC4198744
OpenAlexW2012385481

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.