PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer.
AKT inhibitors
ATP-competitive mTOR inhibitors
Allosteric mTOR inhibitors
Bi-steric mTOR inhibitors
Cancer
Dual PI3K/mTOR inhibitors
Isoform-specific PI3K inhibitors
PDK1 inhibitors
PI3K/AKT/mTORC pathway
Pan PI3K inhibitors
Journal
Molecular cancer
ISSN: 1476-4598
Titre abrégé: Mol Cancer
Pays: England
ID NLM: 101147698
Informations de publication
Date de publication:
18 08 2023
18 08 2023
Historique:
received:
21
05
2023
accepted:
18
07
2023
medline:
21
8
2023
pubmed:
19
8
2023
entrez:
18
8
2023
Statut:
epublish
Résumé
The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed.
Identifiants
pubmed: 37596643
doi: 10.1186/s12943-023-01827-6
pii: 10.1186/s12943-023-01827-6
pmc: PMC10436543
doi:
Substances chimiques
Phosphatidylinositol 3-Kinases
EC 2.7.1.-
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
138Informations de copyright
© 2023. BioMed Central Ltd., part of Springer Nature.
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