M2 muscarinic receptors negatively modulate cell migration in human glioblastoma cells.

Calcium-activated potassium channel Cell migration Glioblastoma Muscarinic acetylcholine receptors

Journal

Neurochemistry international
ISSN: 1872-9754
Titre abrégé: Neurochem Int
Pays: England
ID NLM: 8006959

Informations de publication

Date de publication:
05 Jan 2024
Historique:
received: 08 09 2023
revised: 17 12 2023
accepted: 29 12 2023
medline: 8 1 2024
pubmed: 8 1 2024
entrez: 7 1 2024
Statut: aheadofprint

Résumé

Glioblastoma (GB) is a very aggressive human brain tumor. The high growth potential and invasiveness make this tumor surgically and pharmacologically untreatable. Our previous work demonstrated that the activation of the M2 muscarinic acetylcholine receptors (M2 mAChRs) inhibited cell proliferation and survival in GB cell lines and in the cancer stem cells derived from human biopsies. The aim of the present study was to investigate the ability of M2 mAChR to modulate cell migration in two different GB cell lines: U87 and U251. By wound healing assay and single cell migration analysis performed by time-lapse microscopy, we demonstrated the ability of M2 mAChRs to negatively modulate cell migration in U251 but not in the U87 cell line. In order to explain the different effects observed in the two cell lines we have evaluated the possible involvement of the intermediate conductance calcium-activated potassium (IK

Identifiants

DOI: 10.1016/j.neuint.2023.105673 PMID: 38185384
pubmed: 38185384
pii: S0197-0186(23)00201-2
doi: 10.1016/j.neuint.2023.105673
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

105673

Informations de copyright

Copyright © 2023. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Ada Maria Tata reports article publishing charges was provided by University of Rome La Sapienza. Ada Maria Tata reports a relationship with University of Rome La Sapienza that includes: board membership and funding grants. Ada Maria Tata has patent No patent pending to Not assigned. No conflict of interest to declare.

Auteurs

Claudia Guerriero (C)

Department of Biology and Biotechnologies Charles Darwin, Sapienza University of Rome, 00185, Rome, Italy. Electronic address: claudia.guerriero@uniroma1.it.

Rachele Fanfarillo (R)

Department of Biology and Biotechnologies Charles Darwin, Sapienza University of Rome, 00185, Rome, Italy. Electronic address: fanfarillora@gmail.com.

Patrizia Mancini (P)

Department Experimental Medicine, Sapienza University of Rome, 00185, Rome, Italy. Electronic address: patrizia.mancini@uniroma1.it.

Valentina Sterbini (V)

Institute of Molecular Biology and Pathology, CNR, Rome, Italy. Electronic address: sterbiniv@gmail.com.

Giulia Guarguaglini (G)

Institute of Molecular Biology and Pathology, CNR, Rome, Italy. Electronic address: giulia.guarguaglini@uniroma1.it.

Luigi Sforna (L)

Department of Chemistry Biology and Biotechnology, University of Perugia, 06123, Perugia, Italy. Electronic address: luigi.catacuzzeno@unipg.it.

Antonio Michelucci (A)

Department of Chemistry Biology and Biotechnology, University of Perugia, 06123, Perugia, Italy. Electronic address: antonio.michelucci@unipg.it.

Luigi Catacuzzeno (L)

Department of Chemistry Biology and Biotechnology, University of Perugia, 06123, Perugia, Italy. Electronic address: luigi.sforna@unipg.it.

Ada Maria Tata (AM)

Department of Biology and Biotechnologies Charles Darwin, Sapienza University of Rome, 00185, Rome, Italy; Research Centre of Neurobiology Daniel Bovet, Sapienza University of Rome, 00185, Rome, Italy. Electronic address: adamaria.tata@uniroma1.it.

Classifications MeSH