Evidence map›Paper›PMID 36233192›Full record

ArticleInternational journal of molecular sciences2022

Crosstalk between CXCR4/ACKR3 and EGFR Signaling in Breast Cancer Cells.

Maria Neves, Viviana Marolda, Federico Mayor, Petronila Penela

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Maria NevesDepartment of Molecular Biology, University Institute of Molecular Biology (IUBM-UAM), Centre for Molecular Biology "Severo Ochoa" (CBMSO) UAM-CSIC, Autonomous University of Madrid and Health Research Institute Hospital Universitario La Princesa, 28006 Madrid, Spain.
Viviana MaroldaDepartment of Molecular Biology, University Institute of Molecular Biology (IUBM-UAM), Centre for Molecular Biology "Severo Ochoa" (CBMSO) UAM-CSIC, Autonomous University of Madrid and Health Research Institute Hospital Universitario La Princesa, 28006 Madrid, Spain.
Federico MayorDepartment of Molecular Biology, University Institute of Molecular Biology (IUBM-UAM), Centre for Molecular Biology "Severo Ochoa" (CBMSO) UAM-CSIC, Autonomous University of Madrid and Health Research Institute Hospital Universitario La Princesa, 28006 Madrid, Spain.ORCID 0000-0003-1434-8449
Petronila PenelaDepartment of Molecular Biology, University Institute of Molecular Biology (IUBM-UAM), Centre for Molecular Biology "Severo Ochoa" (CBMSO) UAM-CSIC, Autonomous University of Madrid and Health Research Institute Hospital Universitario La Princesa, 28006 Madrid, Spain.
Centro de Biología Molecular Severo Ochoa · ESInstituto de Salud Carlos III · ES

Funding

Agencia Estatal de Investigación of Spain PID2020-117218RB-I00CIBERCV-Instituto de Salud Carlos III CB16/11/00278Fundación Ramón Areces XX Concurso Nacional para la adjudicación de Ayudas a la Investigación en Ciencias de la Vida y de la MateriaH2020-MSCA Program 860229-ONCORNET 2.0Instituto de Salud Carlos III PI21-01834Programa de Actividades en Biomedicina de la Comunidad de Madrid B2017/BMD-3671-INFLAMUNE
6 · The paper itself

Abstract

A better understanding of the complex crosstalk among key receptors and signaling pathways involved in cancer progression is needed to improve current therapies. We have investigated in cell models representative of the major subtypes of breast cancer (BC) the interplay between the chemokine CXCL12/CXCR4/ACKR3 and EGF receptor (EGFR) family signaling cascades. These cell lines display a high heterogeneity in expression profiles of CXCR4/ACKR3 chemokine receptors, with a predominant intracellular localization and different proportions of cell surface CXCR4+, ACKR3+ or double-positive cell subpopulations, and display an overall modest activation of oncogenic pathways in response to exogenous CXCL12 alone. Interestingly, we find that in MDA-MB-361 (luminal B subtype, Her2-overexpressing), but not in MCF7 (luminal A) or MDA-MB-231 (triple negative) cells, CXCR4/ACKR3 and EGFR receptor families share signaling components and crosstalk mechanisms to concurrently promote ERK1/2 activation, with a key involvement of the G protein-coupled receptor kinase 2 (GRK2) signaling hub and the cytosolic tyrosine kinase Src. Our findings suggest that in certain BC subtypes, a relevant cooperation between CXCR4/ACKR3 and growth factor receptors takes place to integrate concurrent signals emanating from the tumor microenvironment and foster cancer progression.

Indexed as

Breast NeoplasmsReceptors, CXCRReceptors, CXCR4Chemokine CXCL12ErbB ReceptorsFemaleHumansProtein-Tyrosine KinasesSignal TransductionTumor MicroenvironmentACKR3 protein, humanChemokine CXCL12CXCR4 protein, humanEGFR protein, humanErbB ReceptorsProtein-Tyrosine KinasesReceptors, CXCRReceptors, CXCR4ACKR3breast cancerchemokinesCXCL12CXCR4EGF receptorsGRK2Her2MAPK signal crosstalk

Identifiers

PMID36233192
PMCPMC9570020
OpenAlexW4303710002

What Socratic holds

Textmetadata
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.