Evidence map›Paper›PMID 25803821›Full record

ArticlePloS one2015

ABL tyrosine kinase inhibition variable effects on the invasive properties of different triple negative breast cancer cell lines.

Clément Chevalier, Aude Cannet, Simon Descamps, Audrey Sirvent, Valérie Simon, Serge Roche, Christine Benistant

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Graphene quantum dots decorated with imatinib for leukemia treatment.Journal of drug delivery science and technology · 2021
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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

7 authors at 3 institutions in 1 country.

Clément ChevalierCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Aude CannetCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Simon DescampsCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Audrey SirventCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Valérie SimonCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Serge RocheCentre de Recherche de Biochimie Macromoléculaire CNRS UMR5237, University of Montpellier, Montpellier, 34000, France.
Christine BenistantCentre de Biochimie Structurale, CNRS UMR 5048, INSERM UMR 1054, University of Montpellier, Montpellier, 34090, France.
Université de Montpellier · FRCentre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The non-receptor tyrosine kinase ABL drives myeloid progenitor expansion in human chronic myeloid leukemia. ABL inhibition by the tyrosine kinase inhibitor nilotinib is a first-line treatment for this disease. Recently, ABL has also been implicated in the transforming properties of solid tumors, including triple negative (TN) breast cancer. TN breast cancers are highly metastatic and several cell lines derived from these tumors display high invasive activity in vitro. This feature is associated with the activation of actin-rich membrane structures called invadopodia that promote extracellular matrix degradation. Here, we investigated nilotinib effect on the invasive and migratory properties of different TN breast cancer cell lines. Nilotinib decreased both matrix degradation and invasion in the TN breast cancer cell lines MDA-MB 231 and MDA-MB 468. However, and unexpectedly, nilotinib increased by two-fold the invasive properties of the TN breast cancer cell line BT-549 and of Src-transformed fibroblasts. Both display much higher levels of ABL kinase activity compared to MDA-MB 231. Similar effects were obtained by siRNA-mediated down-regulation of ABL expression, confirming ABL central role in this process. ABL anti-tumor effect in BT-549 cells and Src-transformed fibroblasts was not dependent on EGF secretion, as recently reported in neck and squamous carcinoma cells. Rather, we identified the TRIO-RAC1 axis as an important downstream element of ABL activity in these cancer cells. In conclusion, the observation that TN breast cancer cell lines respond differently to ABL inhibitors could have implications for future therapies.

Indexed as

Antineoplastic AgentsAutocrine CommunicationCell Line, TumorCell MovementCell Transformation, NeoplasticFemaleFibroblastsHeparin-binding EGF-like Growth FactorHumansProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrimidinesrac1 GTP-Binding Proteinsrc-Family KinasesTriple Negative Breast NeoplasmsAntineoplastic AgentsHeparin-binding EGF-like Growth FactornilotinibProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrimidinesrac1 GTP-Binding Proteinsrc-Family Kinases

Identifiers

PMID25803821
PMCPMC4372365
OpenAlexW2079094787

What Socratic 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 Socratic graph.