Evidence map›Paper›PMID 37322019›Full record

ArticleNature communications2023

CNK2 promotes cancer cell motility by mediating ARF6 activation downstream of AXL signalling.

Guillaume Serwe, David Kachaner, Jessica Gagnon, Cédric Plutoni, Driss Lajoie, Eloïse Duramé, Malha Sahmi, Damien Garrido, Martin Lefrançois, Geneviève Arseneault and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

14 authors at 1 institution in 1 country.

Guillaume Serwe *Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
David Kachaner *Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Jessica Gagnon *Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Cédric PlutoniInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Driss LajoieInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Eloïse DuraméInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Malha SahmiInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Damien GarridoInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.ORCID 0000-0002-4517-6021
Martin LefrançoisInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Geneviève ArseneaultInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Marc K Saba-El-LeilInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.
Sylvain MelocheInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.ORCID 0000-0002-6201-7786
Gregory EmeryInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada.ORCID 0000-0002-6874-6875
Marc TherrienInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada. marc.therrien@umontreal.ca.ORCID 0000-0003-2047-7650
Institute for Research in Immunology and Cancer · CA

Funding

CIHR FDN-388023CIHR PJT-175093
6 · The paper itself

Abstract

Cell motility is a critical feature of invasive tumour cells that is governed by complex signal transduction events. Particularly, the underlying mechanisms that bridge extracellular stimuli to the molecular machinery driving motility remain partially understood. Here, we show that the scaffold protein CNK2 promotes cancer cell migration by coupling the pro-metastatic receptor tyrosine kinase AXL to downstream activation of ARF6 GTPase. Mechanistically, AXL signalling induces PI3K-dependent recruitment of CNK2 to the plasma membrane. In turn, CNK2 stimulates ARF6 by associating with cytohesin ARF GEFs and with a novel adaptor protein called SAMD12. ARF6-GTP then controls motile forces by coordinating the respective activation and inhibition of RAC1 and RHOA GTPases. Significantly, genetic ablation of CNK2 or SAMD12 reduces metastasis in a mouse xenograft model. Together, this work identifies CNK2 and its partner SAMD12 as key components of a novel pro-motility pathway in cancer cells, which could be targeted in metastasis.

Indexed as

ADP-Ribosylation FactorsNeoplasmsADP-Ribosylation Factor 6AnimalsCell MovementHumansMicePhosphatidylinositol 3-Kinasesrac1 GTP-Binding ProteinSignal TransductionADP-Ribosylation Factor 6ADP-Ribosylation FactorsPhosphatidylinositol 3-Kinasesrac1 GTP-Binding Protein

Identifiers

PMID37322019
PMCPMC10272126
OpenAlexW4380768000

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.