Evidence map›Paper›PMID 28499439›Full record

ReviewCell communication and signaling : CCS2017

The role of TGF-β and its crosstalk with RAC1/RAC1b signaling in breast and pancreas carcinoma.

Catharina Melzer, Ralf Hass, Juliane von der Ohe, Hendrik Lehnert, Hendrik Ungefroren

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  8. Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024
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  9. The role of cuproptosis in gastric cancer.Frontiers in immunology · 2024
    Review
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  11. Directing the migration of serum-free,Frontiers in immunology · 2024
    Article
  12. Enhanced fibrotic potential of COL1A1Frontiers in cardiovascular medicine · 2024
    Article
  13. Review
  14. Review
  15. Article
  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

5 authors at 3 institutions in 1 country.

Catharina MelzerBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Ralf HassBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Juliane von der OheBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Hendrik LehnertCenter of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Campus Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany.
Hendrik UngefrorenCenter of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Campus Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany. hendrik.ungefroren@uksh.de.ORCID 0000-0002-7552-2087
Medizinische Hochschule Hannover · DEHochschule für Angewandte Wissenschaften Kiel · DEUniversitäres Kinderwunschzentrum Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. These processes are controlled entirely or in part by TGF-β and the small RHO GTPase RAC1 with both proteins acting as tumor promoters in late-stage cancers. Data from our and other studies point to signaling crosstalk between TGF-β and RAC1 and the related isoform, RAC1b, in pancreatic and mammary carcinoma cells. Based on the exciting observation that RAC1b functions as an endogenous inhibitor of RAC1, we propose a model on how the relative abundance or activity of RAC1 and RAC1b in the tumor cells may determine their responses to TGF-β and, ultimately, the metastatic capacity of the tumor.

Indexed as

Signal TransductionAnimalsBreast NeoplasmsHumansPancreatic Neoplasmsrac1 GTP-Binding ProteinTransforming Growth Factor betarac1 GTP-Binding ProteinRAC1 protein, humanTransforming Growth Factor betaBreast cancerMetastasisPancreas cancerRac1TGF-βTumor cell signalingTumor microenvironment

Identifiers

PMID28499439
PMCPMC5429551
OpenAlexW2613659776

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.