Activating p53 function by targeting RLIP.
Drug resistance
Glutathione-electrophile conjugate
Mercapturic acid pathway
Metastasis
PKCα
RLIP
RalBP1
Therapeutics
p53
Journal
Biochimica et biophysica acta. Reviews on cancer
ISSN: 1879-2561
Titre abrégé: Biochim Biophys Acta Rev Cancer
Pays: Netherlands
ID NLM: 9806362
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
25
12
2020
revised:
06
01
2021
accepted:
07
01
2021
pubmed:
19
1
2021
medline:
20
7
2021
entrez:
18
1
2021
Statut:
ppublish
Résumé
Aberrations in RLIP, p53, and PKCα represent essentially the entire spectrum of all human neoplasms. Elevated PKCα expression, failure of the cell cycle checkpoint (p53 dysfunction), and abnormal glutathione (GSH) metabolism are fundamental hallmarks of carcinogenesis and drug/radiation resistance. However, a lack of investigations into the interactions between these important regulatory nodes has fundamentally limited our understanding of carcinogenesis and the development of effective interventions for cancer prevention and therapy. Loss of p53, perhaps the most powerful tumor suppressor gene, predisposes rodents to spontaneous cancer and humans to familial, as well as acquired, cancers. Until recently, no genetic manipulation of any oncogene had been reported to abrogate spontaneous carcinogenesis in p53
Identifiants
pubmed: 33460725
pii: S0304-419X(21)00011-1
doi: 10.1016/j.bbcan.2021.188512
pmc: PMC9082734
mid: NIHMS1796787
pii:
doi:
Substances chimiques
ATP-Binding Cassette Transporters
0
GTPase-Activating Proteins
0
RALBP1 protein, human
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
PRKCA protein, human
EC 2.7.11.13
Protein Kinase C-alpha
EC 2.7.11.13
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
188512Subventions
Organisme : NCI NIH HHS
ID : P30 CA033572
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier B.V. All rights reserved.
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