The Dual Roles of the Atypical Protein Kinase Cs in Cancer.
Animals
Antineoplastic Agents
/ pharmacology
Cell Polarity
/ genetics
Cell Transformation, Neoplastic
/ drug effects
Disease Models, Animal
Epithelial Cells
/ metabolism
Gene Expression Regulation, Neoplastic
/ drug effects
Humans
Isoenzymes
/ antagonists & inhibitors
Mice, Transgenic
Mutation
Neoplasms
/ drug therapy
Protein Kinase C
/ antagonists & inhibitors
Protein Kinase Inhibitors
/ pharmacology
Proto-Oncogenes
/ genetics
Signal Transduction
/ drug effects
Tumor Microenvironment
/ genetics
Tumor Suppressor Proteins
/ genetics
ECT2
Hedgehog
PD-L1
PHGDH
PKCζ
PKCλ/ι
SOX2
atypical PKCs
basal cell carcinoma
cancer
colorectal cancer
immunotherapy
kinase inhibitors
leukemia
lung cancer
metabolism
p62
polarity
prostate cancer
stroma
tumor promoter
tumor suppressor
Journal
Cancer cell
ISSN: 1878-3686
Titre abrégé: Cancer Cell
Pays: United States
ID NLM: 101130617
Informations de publication
Date de publication:
16 09 2019
16 09 2019
Historique:
received:
20
05
2019
revised:
24
06
2019
accepted:
30
07
2019
pubmed:
3
9
2019
medline:
19
5
2020
entrez:
3
9
2019
Statut:
ppublish
Résumé
Atypical protein kinase C (aPKC) isozymes, PKCλ/ι and PKCζ, are now considered fundamental regulators of tumorigenesis. However, the specific separation of functions that determine their different roles in cancer is still being unraveled. Both aPKCs have pleiotropic context-dependent functions that can translate into tumor-promoter or -suppressive functions. Here, we review early and more recent literature to discuss how the different tumor types, and their microenvironments, might account for the selective signaling of each aPKC isotype. This is of clinical relevance because a better understanding of the roles of these kinases is essential for the design of new anti-cancer treatments.
Identifiants
pubmed: 31474570
pii: S1535-6108(19)30337-X
doi: 10.1016/j.ccell.2019.07.010
pmc: PMC6751000
mid: NIHMS1536574
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Isoenzymes
0
Protein Kinase Inhibitors
0
Tumor Suppressor Proteins
0
protein kinase C zeta
EC 2.7.11.1
Protein Kinase C
EC 2.7.11.13
protein kinase C lambda
EC 2.7.11.13
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
218-235Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK108743
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA211794
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA207177
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA192642
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA218254
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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