Mechanisms of action of NME metastasis suppressors - a family affair.
Channeling
Dynamin
GTP
Metastasis
Nucleoside diphosphate kinase
Journal
Cancer metastasis reviews
ISSN: 1573-7233
Titre abrégé: Cancer Metastasis Rev
Pays: Netherlands
ID NLM: 8605731
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
received:
04
04
2023
accepted:
09
06
2023
pubmed:
24
6
2023
medline:
24
6
2023
entrez:
23
6
2023
Statut:
ppublish
Résumé
Metastatic progression is regulated by metastasis promoter and suppressor genes. NME1, the prototypic and first described metastasis suppressor gene, encodes a nucleoside diphosphate kinase (NDPK) involved in nucleotide metabolism; two related family members, NME2 and NME4, are also reported as metastasis suppressors. These proteins physically interact with members of the GTPase dynamin family, which have key functions in membrane fission and fusion reactions necessary for endocytosis and mitochondrial dynamics. Evidence supports a model in which NDPKs provide GTP to dynamins to maintain a high local GTP concentration for optimal dynamin function. NME1 and NME2 are cytosolic enzymes that provide GTP to dynamins at the plasma membrane, which drive endocytosis, suggesting that these NMEs are necessary to attenuate signaling by receptors on the cell surface. Disruption of NDPK activity in NME-deficient tumors may thus drive metastasis by prolonging signaling. NME4 is a mitochondrial enzyme that interacts with the dynamin OPA1 at the mitochondria inner membrane to drive inner membrane fusion and maintain a fused mitochondrial network. This function is consistent with the current view that mitochondrial fusion inhibits the metastatic potential of tumor cells whereas mitochondrial fission promotes metastasis progression. The roles of NME family members in dynamin-mediated endocytosis and mitochondrial dynamics and the intimate link between these processes and metastasis provide a new framework to understand the metastasis suppressor functions of NME proteins.
Identifiants
pubmed: 37353690
doi: 10.1007/s10555-023-10118-x
pii: 10.1007/s10555-023-10118-x
pmc: PMC10713741
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1155-1167Informations de copyright
© 2023. The Author(s).
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