MAPK inhibitors dynamically affect melanoma release of immune NKG2D-ligands, as soluble protein and extracellular vesicle-associated.
extracellular vesicles
immune evasion
immunomodulation
metalloproteases
metastatic melanoma
targeted cancer therapy
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
27
09
2022
accepted:
13
12
2022
entrez:
2
2
2023
pubmed:
3
2
2023
medline:
3
2
2023
Statut:
epublish
Résumé
Metastatic melanoma presents, in many cases, oncogenic mutations in BRAF, a MAPK involved in proliferation of tumour cells. BRAF inhibitors, used as therapy in patients with these mutations, often lead to tumour resistance and, thus, the use of MEK inhibitors was introduced in clinics. BRAFi/MEKi, a combination that has modestly increased overall survival in patients, has been proven to differentially affect immune ligands, such as NKG2D-ligands, in drug-sensitive vs. drug-resistant cells. However, the fact that NKG2D-ligands can be released as soluble molecules or in extracellular vesicles represents an additional level of complexity that has not been explored. Here we demonstrate that inhibition of MAPK using MEKi, and the combination of BRAFi with MEKi
Identifiants
pubmed: 36726591
doi: 10.3389/fcell.2022.1055288
pii: 1055288
pmc: PMC9884675
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1055288Informations de copyright
Copyright © 2023 López-Borrego, Campos-Silva, Sandúa, Camino, Téllez-Pérez, Alegre, Beneitez, Jara-Acevedo, Paschen, Pardo, González and Valés-Gómez.
Déclaration de conflit d'intérêts
RJ-A is CEO in Immunostep, S.L. AB is employee of Immunostep, S.L. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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