Evidence map›Paper›PMID 26091707›Full record

ArticleJournal of cancer research and clinical oncology2016

Role of dihydrotestosterone (DHT) on TGF-β1 signaling pathway in epithelial ovarian cancer cells.

Karla Kohan-Ivani, Fernando Gabler, Alberto Selman, Margarita Vega, Carmen Romero

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2016. 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
1.1field-weighted citation impact, top 24% 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, 24 citations in OpenAlex.

  1. A Natural Inhibitor, 1'Molecules (Basel, Switzerland) · 2025
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. TGFβ Controls Ovarian Cancer Cell Proliferation.International journal of molecular sciences · 2017
    Review
  15. 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

5 authors at 3 institutions in 1 country.

Karla Kohan-IvaniLaboratory of Endocrinology and Reproductive Biology, University of Chile Clinical Hospital, Avda. Santos Dumont # 999, Independencia, Santiago, Chile.
Fernando GablerDepartment of Pathology, School of Medicine, San Borja Arriarán Clinical Hospital, University of Chile, Santiago, Chile.
Alberto SelmanDepartment of Obstetrics and Gynecology, School of Medicine, University of Chile Clinical Hospital, Santiago, Chile.
Margarita VegaLaboratory of Endocrinology and Reproductive Biology, University of Chile Clinical Hospital, Avda. Santos Dumont # 999, Independencia, Santiago, Chile.
Carmen RomeroLaboratory of Endocrinology and Reproductive Biology, University of Chile Clinical Hospital, Avda. Santos Dumont # 999, Independencia, Santiago, Chile. cromero@hcuch.cl.
University of Chile · CLHospital Clínico de la Universidad de Chile · CLHospital San Borja Arriarán · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeOne of the hypotheses regarding the genesis of epithelial ovarian cancer involves the action of androgens on the proliferation of epithelial ovarian cells, as well as inclusion cysts. The purpose of the present study was to evaluate whether DHT causes changes in the TGF-β1 pathway that might modify the anti-proliferative effect of the latter.

methodsThe levels of TGF-β1 protein, of its receptors (TGFBR1 and TGFBR2), of Smad2/3 (canonical signaling pathway protein) and of p21 (cell cycle protein) were assessed in ovarian tissues, epithelial ovarian cancer cell lines (A2780) and control cell lines (HOSE) through the use of immunohistochemistry and immunocytochemistry. Additionally, cell lines were treated with 100 nmol/L DHT, 10 ng/mL of TGF-β1 and DHT + TGF-β1 during 72 h in the presence and absence of a siRNA against androgen receptor. After treatment, TGFBR1 and TGFBR2 levels were detected through Western blotting and p21 was assessed through immunocytochemistry.

resultsEpithelial ovarian cancer tissues showed a decrease in TGF-β1 I receptor (p < 0.05) and a change in Smad2/3 protein levels. Additionally, after treatment of cell lines with DHT, protein levels of TGF-β1 receptors (TGFBR1-TGFBR2) showed a decrease (p < 0.05) that might cause a potential disorder in TGF-β1 response, represented by the significant decrease in p21 protein levels in the presence of DHT (p < 0.001).

conclusionsOverall, our results indicate a defect in the canonical TGF-β signaling pathway in epithelial ovarian cancer caused by androgen action, thus suggesting eventual changes in such tissue proliferation rates.

Indexed as

AndrogensApoptosisBlotting, WesternCarcinoma, Ovarian EpithelialCell ProliferationCyclin-Dependent Kinase Inhibitor p21DihydrotestosteroneFemaleGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesNeoplasms, Glandular and EpithelialOvarian NeoplasmsOvaryProtein Serine-Threonine KinasesReal-Time Polymerase Chain ReactionAndrogensAR protein, humanCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DihydrotestosteroneProtein Serine-Threonine KinasesReceptors, AndrogenReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIRNA, MessengerSmad2 ProteinSMAD2 protein, humanTGFBR1 protein, humanTransforming Growth Factor beta1Androgen receptorEpithelial ovarian cancerTGF-β signaling pathway

Identifiers

PMID26091707
PMCPMC4705116
OpenAlexW658783899

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.