Evidence map›Paper›PMID 23783250›Full record

ArticleMolecular cancer therapeutics2013

An autocrine loop between TGF-β1 and the transcription factor brachyury controls the transition of human carcinoma cells into a mesenchymal phenotype.

Cecilia Larocca, Joseph R Cohen, Romaine I Fernando, Bruce Huang, Duane H Hamilton, Claudia Palena

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2013. 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
3.6field-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

44 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Fine-Tuned Expression of Evolutionarily Conserved Signaling Molecules in theInternational journal of molecular sciences · 2024
    Article
  4. Chordoma cells possess bone-dissolving activity at the bone invasion front.Cellular oncology (Dordrecht, Netherlands) · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. New Prospects for Molecular Targets for Chordomas.Neurosurgery clinics of North America · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. 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 1 institution in 1 country.

Cecilia LaroccaCorresponding Author: Claudia Palena, Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH; 10 Center Drive, Room 8B14, MSC 1750, Bethesda, MD 20892. palenac@mail.nih.gov.
Joseph R Cohen
Romaine I Fernando
Bruce Huang
Duane H Hamilton
Claudia Palena
National Cancer Institute · US

Funding

Novel Targets for Vaccine TherapyZICBC010937 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PALENA, CLAUDIA · 2010 to 2022
$13.2M
Intramural NIH HHS ZIC BC010937
6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is a process associated with the metastasis of solid tumors as well as with the acquisition of resistance to standard anticancer modalities. A major initiator of EMT in carcinoma cells is TGF-β, which has been shown to induce the expression of several transcription factors ultimately responsible for initiating and maintaining the EMT program. We have previously identified Brachyury, a T-box transcription factor, as an inducer of mesenchymal features in human carcinoma cells. In this study, a potential link between Brachyury and TGF-β signaling has been investigated. The results show for the first time that Brachyury expression is enhanced during TGF-β1-induced EMT in various human cancer cell lines, and that a positive feedback loop is established between Brachyury and TGF-β1 in mesenchymal-like tumor cells. In this context, Brachyury overexpression is shown to promote upregulation of TGF-β1 at the mRNA and protein levels, an effect mediated by activation of the TGF-β1 promoter in the presence of high levels of Brachyury. Furthermore, inhibition of TGF-β1 signaling by a small-molecule inhibitor of TGF-β receptor type I decreases Brachyury expression, induces a mesenchymal-to-epithelial transition, and renders cancer cells more susceptible to chemotherapy. This study thus has implications for the future development of clinical trials using TGF-β inhibitors in combination with other anticancer agents.

Indexed as

Epithelial-Mesenchymal TransitionAntineoplastic Combined Chemotherapy ProtocolsBrachyury ProteinCell Line, TumorCisplatinDrug Evaluation, PreclinicalDrug Resistance, NeoplasmFeedback, PhysiologicalFetal ProteinsGene Expression Regulation, NeoplasticHumansNeoplasmsPhenotypePteridinesReceptors, Transforming Growth Factor betaSignal TransductionBrachyury ProteinCisplatinFetal ProteinsPteridinesReceptors, Transforming Growth Factor betaSD-208T-Box Domain ProteinsTransforming Growth Factor beta1VinblastineVinorelbine

Identifiers

PMID23783250
PMCPMC3815539
OpenAlexW2102124205

What OpenQuestion holds

Textmetadata
LicenceTDM
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.