Evidence map›Paper›PMID 29379163›Full record

ArticleOncogene2018

c-Src activity is differentially required by cancer cell motility modes.

Jeremy S Logue, Alexander X Cartagena-Rivera, Richard S Chadwick

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Amoeboid cancer cells at a glance.Journal of cell science · 2026
    Review
  3. Article
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  7. Article
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  10. Article
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  13. The molecular and clinical role of Tensin 1/2/3 in cancer.Journal of cellular and molecular medicine · 2023
    Review
  14. Article
  15. Article
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  18. Review
  19. 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

3 authors at 2 institutions in 1 country.

Jeremy S LogueNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. loguej@mail.amc.edu.
Alexander X Cartagena-RiveraNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
Richard S ChadwickNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
National Institute on Deafness and Other Communication Disorders · USNational Institutes of Health · US

Funding

Biomechanics Of Cochlear Fine TuningZIADC000033 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI CHADWICK, RICHARD S. · 2009 to 2019
$8.4M
6 · The paper itself

Abstract

Cancer cell migration requires that cells respond and adapt to their surroundings. In the absence of extracellular matrix cues, cancer cells will undergo a mesenchymal to ameboid transition, whereas a highly confining space will trigger a switch to "leader bleb-based" migration. To identify oncogenic signaling pathways mediating these transitions, we undertook a targeted screen using clinically useful inhibitors. Elevated Src activity was found to change actin and focal adhesion dynamics, whereas inhibiting Src triggered focal adhesion disassembly and blebbing. On non-adherent substrates and in collagen matrices, amoeboid-like, blebbing cells having high Src activity formed protrusions of the plasma membrane. To evaluate the role of Src in confined cells, we use a novel approach that places cells under a slab of polydimethylsiloxane (PDMS), which is held at a defined height. Using this method, we find that leader bleb-based migration is resistant to Src inhibition. High Src activity was found to markedly change the architecture of cortical actomyosin, reduce cell mechanical properties, and the percentage of cells that undergo leader bleb-based migration. Thus, Src is a signal transducer that can potently influence transitions between migration modes with implications for the rational development of metastasis inhibitors.

Indexed as

Cell MovementActinsAmino Acid SubstitutionButadienesCell AdhesionDasatinibHumansImidazolesMutant ProteinsNeoplasmsNitrilesPhosphorylcholineProtein Kinase InhibitorsProto-Oncogene Proteins pp60(c-src)QuinolinesTumor Cells, CulturedActinsButadienesdactolisibDasatinibImidazolesMutant ProteinsNitrilesperifosinePhosphorylcholineProtein Kinase InhibitorsProto-Oncogene Proteins pp60(c-src)QuinolinesU 0126

Identifiers

PMID29379163
PMCPMC5906457
OpenAlexW2792613799

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.