Evidence map›Paper›PMID 31108998›Full record

ArticleCancers2019

RAC1B Suppresses TGF-β1-Dependent Cell Migration in Pancreatic Carcinoma Cells through Inhibition of the TGF-β Type I Receptor ALK5.

Hendrik Ungefroren, Hannah Otterbein, Christian Fiedler, Koichiro Mihara, Morley D Hollenberg, Frank Gieseler, Hendrik Lehnert, David Witte

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. 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
1.5field-weighted citation impact, top 16% 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, 23 citations in OpenAlex.

  1. Review
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  3. Article
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  8. Article
  9. Review
  10. RAC1B Regulation ofCancers · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Article
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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

8 authors at 2 institutions in 2 countries.

Hendrik UngefrorenFirst Department of Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. hendrik.ungefroren@uksh.de.ORCID 0000-0002-7552-2087
Hannah OtterbeinFirst Department of Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. hannahotterbein@web.de.
Christian FiedlerFirst Department of Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. c.fiedler93@gmx.de.
Koichiro MiharaDepartments of Physiology and Pharmacology and Medicine, Inflammation Research Network, Snyder Institute for Chronic Diseases, University of Calgary, Cumming School of Medicine, Calgary, AB T2N 4N1, Canada. mihara@ucalgary.ca.ORCID 0000-0002-8927-060X
Morley D HollenbergDepartments of Physiology and Pharmacology and Medicine, Inflammation Research Network, Snyder Institute for Chronic Diseases, University of Calgary, Cumming School of Medicine, Calgary, AB T2N 4N1, Canada. mhollenb@ucalgary.ca.
Frank GieselerDepartment of Oncology, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. frank.gieseler@uksh.de.ORCID 0000-0001-6409-3822
Hendrik LehnertFirst Department of Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. hendrik.lehnert@uni-luebeck.de.
David WitteFirst Department of Medicine, University Hospital Schleswig-Holstein, Campus Lübeck, D-23538 Lübeck, Germany. davidwittemail@gmail.com.
University Hospital Schleswig-Holstein · DEUniversity of Calgary · CA

Funding

Canadian Institutes of Health Research PJT148565 to M.D.H.
6 · The paper itself

Abstract

The small GTPase Ras-related C3 botulinum toxin substrate 1B (RAC1B) has been shown previously by RNA interference-mediated knockdown (KD) to function as a powerful inhibitor of transforming growth factor (TGF)-β1-induced cell migration and epithelial-mesenchymal transition in epithelial cells, but the underlying mechanism has remained enigmatic. Using pancreatic carcinoma cells, we show that both KD and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9-mediated knockout (KO) of RAC1B increased the expression of the TGF-β type I receptor ALK5 (activin receptor-like kinase 5), but this effect was more pronounced in CRISPR-KO cells. Of note, in KO, but not KD cells, ALK5 upregulation was associated with resensitization of

Indexed as

ALK5cell migrationCRISPR/Cas9pancreatic carcinomaRAC1BRNA interferenceTGF-β

Identifiers

PMID31108998
PMCPMC6562819
OpenAlexW2944998961

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.