Evidence map›Paper›PMID 25243859›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

TGFβ signaling promotes juvenile granulosa cell tumorigenesis by suppressing apoptosis.

Nadéra Mansouri-Attia, Swamy K Tripurani, Nisha Gokul, Hermann Piard, Matthew L Anderson, Karen Eldin, Stephanie A Pangas

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. The TGF-β Family in the Reproductive Tract.Cold Spring Harbor perspectives in biology · 2017
    Review
  8. Follistatin is critical for mouse uterine receptivity and decidualization.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Review
  11. Article
  12. The SMAD2/3 pathway is involved in hepaCAM-induced apoptosis by inhibiting the nuclear translocation of SMAD2/3 in bladder cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  13. Article
  14. Review
  15. 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 1 institution in 1 country.

Nadéra Mansouri-AttiaDepartment of Pathology and Immunology (N.M.-A., S.K.T., H.P., M.L.A., K.E., S.A.P.), Department of Obstetrics and Gynecology (M.L.A.), Graduate Program in Molecular and Cell Biology (N.G.), and Department of Molecular and Cellular Biology (S.A.P.), Baylor College of Medicine, Houston, Texas 77030.
Swamy K Tripurani
Nisha Gokul
Hermann Piard
Matthew L Anderson
Karen Eldin
Stephanie A Pangas
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
Role of the BMP SMADs in OncogenesisR01CA138628 · NCI · BAYLOR COLLEGE OF MEDICINE · PI PANGAS, STEPHANIE A. · 2010 to 2014
$1.5M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS CA125123NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA138628NCRR NIH HHS RR024574NCRR NIH HHS S10 RR024574NIAID NIH HHS AI036211NIAID NIH HHS P30 AI036211
6 · The paper itself

Abstract

Molecular changes that give rise to granulosa cell tumors of the ovary are not well understood. Previously, we showed that deletion in granulosa cells of the bone morphogenetic protein receptor-signaling transcription factors, Smad1 and Smad5, causes development of metastatic granulosa cell tumors that phenocopy the juvenile form of granulosa cell tumors (JGCTs) in humans. The TGFβ-SMAD2/3 pathway is active in JGCTs, but its role is unknown. We tested the in vivo contribution of TGFβ-SMAD signaling to JGCT development by genetically deleting the common Smad4 from Smad1/5 double knockout mice. Smad1/5/4 triple knockout mice were sterile and had significantly increased survival and delayed tumor development compared to those for the Smad1/5 double knockout mice. The few tumors that did develop were smaller, showed no evidence of metastasis, and had increased apoptosis. In the human JGCT cell line COV434, TGFβ1 increased viability by inhibiting apoptosis through a TGFβ type I receptor-dependent repression of caspase activity and inhibition of poly(ADP-ribose) polymerase cleavage. These data support a tumor-promoting function of TGFβ in JGCTs through its ability to repress apoptosis.

Indexed as

AnimalsApoptosisCarcinogenesisCell SurvivalCell Transformation, NeoplasticFemaleGranulosa CellsGranulosa Cell TumorHumansMaleMiceMice, Inbred C57BLMice, KnockoutPoly(ADP-ribose) PolymerasesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaPoly(ADP-ribose) PolymerasesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad ProteinsTransforming Growth Factor beta1

Identifiers

PMID25243859
PMCPMC4213364
OpenAlexW2078875366

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.