Evidence map›Paper›PMID 17066266›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2007

Proliferation and cell-cell fusion of endometrial carcinoma are induced by the human endogenous retroviral Syncytin-1 and regulated by TGF-beta.

Reiner Strick, Sven Ackermann, Manuela Langbein, Justine Swiatek, Steffen W Schubert, Said Hashemolhosseini, Thomas Koscheck, Peter A Fasching, Ralf L Schild, Matthias W Beckmann and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 6% 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

94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The double-positive cells in the tumor microenvironment.Journal of translational internal medicine · 2026
    Article
  4. Review
  5. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
    Review
  6. How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026
    Review
  7. Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  8. Spectrum and Impact of Mitochondrial DNA Mutations in Ovarian Cancer.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024
    Review
  17. Article
  18. Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024
    Review
  19. Mechanisms of Cell Fusion in Cancer.Results and problems in cell differentiation · 2024
    Review
  20. Article

34 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

Reiner StrickDepartment of Gynaecology and Obstetrics, Laboratory for Molecular Medicine, University Clinic Erlangen, Universitaetsstr. 21-23, 91054, Erlangen, Germany. Reiner.Strick@gyn.imed.uni-erlangen.de
Sven Ackermann
Manuela Langbein
Justine Swiatek
Steffen W Schubert
Said Hashemolhosseini
Thomas Koscheck
Peter A Fasching
Ralf L Schild
Matthias W Beckmann
Pamela L Strissel
Universitätsklinikum Erlangen · DEUniversity Radiology · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial carcinomas (EnCa) predominantly represent a steroid hormone-driven tumor initiated from prestages. The human endogenous retrovirus HERV-W envelope gene Syncytin-1 was significantly increased at the mRNA and protein levels in EnCa and prestages compared to controls. Steroid hormone treatment of primary EnCa cells and cell lines induced Syncytin-1 due to a new HERV-W estrogen response element and resulted in increased proliferation. Activation of the cAMP-pathway also resulted in Syncytin-1 upregulation, but in contrast to proliferation, classic cell-cell fusions similar to placental syncytiotrophoblasts occurred. Cell-cell fusions were also histologically identified in endometrioid EnCa tumors in vivo. Clonogenic soft agar experiments showed that Syncytin-1 is also involved in anchorage-independent colony growth as well as in colony fusions depending on steroid hormones or cAMP-activation. The posttranscriptional silencing of Syncytin-1 gene expression and a concomitant functional block of induced cell proliferation and cell-cell fusion with siRNAs proved the essential role of Syncytin-1 in these cellular processes. TGF-beta1 and TGF-beta3 were identified as main regulative factors, due to the finding that steroid hormone inducible TGF-beta1 and TGF-beta3 inhibited cell-cell fusion, whereas antibody-mediated TGF-beta neutralization induced cell-cell fusions. These results showed that induced TGF-beta could override Syncytin-1-mediated cell-cell fusions. Interactions between Syncytin-1 and TGF-beta may contribute to the etiology of EnCa progression and also help to clarify the regulation of cell-cell fusions occurring in development and in other syncytial cell tumors.

Indexed as

Cell ProliferationAdultAgedAged, 80 and overApoptosisBlotting, NorthernBlotting, SouthernBlotting, WesternCell FusionEndometrial NeoplasmsFemaleGene Expression ProfilingGene Products, envGene SilencingHumansImmunoblottingGene Products, envPregnancy ProteinsRNA, MessengersyncytinTransforming Growth Factor beta

Identifiers

PMID17066266
OpenAlexW1972816098

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.