CXCR7 contributes to the aggressive phenotype of cholangiocarcinoma cells.

Bile Duct Neoplasms / metabolism Cell Movement Cell Survival Chemokine CXCL12 / metabolism Cholangiocarcinoma / metabolism Female Humans Liver / metabolism Male Phenotype RNA Interference RNA, Small Interfering / metabolism Receptors, CXCR / antagonists & inhibitors Tumor Cells, Cultured beta-Arrestin 2 / metabolism
Cancer stem cells Cell migration Chemokines Liver stromal cells β-Arrestin 2

Journal

Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730

Informations de publication

Date de publication:
01 09 2019
Historique:
received: 23 02 2018
revised: 20 12 2018
accepted: 06 01 2019
pubmed: 7 5 2019
medline: 8 5 2020
entrez: 7 5 2019
Statut: ppublish

Résumé

Development of cholangiocarcinoma (CCA) is dependent on a cross-talk with stromal cells, which release different chemokines including CXCL12, that interacts with two different receptors, CXCR4 and CXCR7. The aim of the present study was to investigate the role of CXCR7 in CCA cells. CXCR7 is overexpressed by different CCA cell lines and in human CCA specimens. Knock-down of CXCR7 in HuCCT-1 cells reduced migration, invasion, and CXCL12-induced adhesion to collagen I. Survival of CCA was also reduced in CXCR7-silenced cells. The ability of CXCL12 to induce cell migration and survival was also blocked by CCX733, a CXCR7 antagonist. Similar effects of CXCR7 activation were observed in CCLP-1 cells and in primary iCCA cells. Enrichment of tumor stem-like cells by a 3D culture system resulted in increased CXCR7 expression compared to cells grown in monolayers, and genetic knockdown of CXCR7 robustly reduced sphere formation both in HuCCT-1 and in CCLP-1 cells. In HuCCT-1 cells CXCR7 was found to interact with β-arrestin 2, which was necessary to mediate CXCL12-induced migration, but not survival. In conclusion, CXCR7 is widely expressed in CCA, and contributes to the aggressive phenotype of CCA cells, inducing cell migration, invasion, adhesion, survival, growth and stem cell-like features. Cell migration induced by CXCR7 requires interaction with β-arrestin 2.

Identifiants

DOI: 10.1016/j.bbadis.2019.04.020 PMID: 31059778
pubmed: 31059778
pii: S0925-4439(19)30148-6
doi: 10.1016/j.bbadis.2019.04.020
pii:
doi:

Substances chimiques

ACKR3 protein, human 0
CXCL12 protein, human 0
Chemokine CXCL12 0
RNA, Small Interfering 0
Receptors, CXCR 0
beta-Arrestin 2 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2246-2256

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Alessandra Gentilini (A)

Department of Experimental and Clinical Medicine, University of Florence, Italy. Electronic address: alessandra.gentilini@unifi.it.

Alessandra Caligiuri (A)

Department of Experimental and Clinical Medicine, University of Florence, Italy. Electronic address: alessandra.caligiuri@unifi.it.

Chiara Raggi (C)

Department of Experimental and Clinical Medicine, University of Florence, Italy; Center for Autoimmune Liver Diseases IRCCS Istituto Clinico Humanitas, Rozzano, MI, Italy. Electronic address: chiara.raggi@unifi.it.

Krista Rombouts (K)

University College London (UCL), Institute for Liver and Digestive Health, Royal Free Hospital, London, UK. Electronic address: k.rombouts@ucl.ac.uk.

Massimo Pinzani (M)

University College London (UCL), Institute for Liver and Digestive Health, Royal Free Hospital, London, UK. Electronic address: m.pinzani@ucl.ac.uk.

Giulia Lori (G)

Department of Experimental and Clinical Medicine, University of Florence, Italy. Electronic address: giulia.lori@unifi.it.

Margherita Correnti (M)

Center for Autoimmune Liver Diseases IRCCS Istituto Clinico Humanitas, Rozzano, MI, Italy. Electronic address: Margherita.Correntii@humanitasresearch.it.

Pietro Invernizzi (P)

University of Milan Bicocca, Milan, Italy. Electronic address: pietro.invernizzi@unimib.it.

Elisabetta Rovida (E)

Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Italy. Electronic address: elisabetta.rovida@unifi.it.

Nadia Navari (N)

Department of Experimental and Clinical Medicine, University of Florence, Italy. Electronic address: nadia.navari@unifi.it.

Sabina Di Matteo (S)

Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy. Electronic address: sabina.dimatteo@uniroma1.it.

Domenico Alvaro (D)

Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy. Electronic address: domenico.alvaro@uniroma1.it.

Jesus M Banales (JM)

Department of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, CIBERehd, Ikerbasque, San Sebastian, Spain. Electronic address: JESUS.BANALES@biodonostia.org.

Pedro Rodrigues (P)

Department of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, CIBERehd, Ikerbasque, San Sebastian, Spain. Electronic address: PEDRO.RODRIGUES@biodonostia.org.

Carlotta Raschioni (C)

Oncology Experimental Therapeutics, Humanitas Clinical and Research Center, Rozzano, Milan, Italy. Electronic address: carlotta.raschioni@gmail.com.

Matteo Donadon (M)

Department of Pathology, IRCCS Humanitas Clinical Institute, Rozzano, MI, Italy. Electronic address: matteo.donadon@humanitas.it.

Luca Di Tommaso (L)

Pathology Unit, Humanitas Clinical and Research Center, Rozzano, MI, Italy; Department of Biomedical Sciences, Humanitas University, Rozzano, MI, Italy. Electronic address: luca.di_tommaso@hunimed.eu.

Fabio Marra (F)

Department of Experimental and Clinical Medicine, University of Florence, Italy. Electronic address: fabio.marra@unifi.it.

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Classifications MeSH

questionsmedicales.fr › Maladies de l'appareil digestif › Tumeurs de l'appareil digestif › Tumeurs des voies biliaires › Tumeurs des canaux biliaires › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Phénomènes physiologiques › Mouvement cellulaire › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Survie cellulaire › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Chimiokines › Chimiokines CXC › Chimiokine CXCL12 › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Tumeurs › Tumeurs par type histologique › Tumeurs épithéliales épidermoïdes et glandulaires › Carcinomes › Adénocarcinome › Cholangiocarcinome › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Système digestif › Foie › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Phénomènes génétiques › Phénotype › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Épigenèse génétique › Extinction de l'expression des gènes › Interférence par ARN › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN non traduit › Petit ARN non traduit › Petit ARN interférent › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Récepteurs aux cytokines › Récepteurs aux chimiokines › Récepteurs CXCR › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Cellules › Cellules cultivées › Cellules cancéreuses en culture › CXCR7 contributes to the aggressive phenotype...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Arrestines › bêta-Arrestines › bêta-Arrestine 2 › CXCR7 contributes to the aggressive phenotype...