Loss of wild-type p53 promotes mutant p53-driven metastasis through acquisition of survival and tumor-initiating properties.
Animals
Carcinogenesis
/ genetics
Cell Line, Tumor
Cell Survival
Clone Cells
Cluster Analysis
Female
Gain of Function Mutation
Humans
Inflammation
/ pathology
Intestinal Neoplasms
/ pathology
Liver Neoplasms
/ secondary
Loss of Heterozygosity
MAP Kinase Signaling System
Mice
Mutation
/ genetics
Organoids
/ pathology
Tumor Suppressor Protein p53
/ genetics
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
11 05 2020
11 05 2020
Historique:
received:
03
08
2019
accepted:
23
04
2020
entrez:
13
5
2020
pubmed:
13
5
2020
medline:
6
8
2020
Statut:
epublish
Résumé
Missense-type mutant p53 plays a tumor-promoting role through gain-of-function (GOF) mechanism. In addition, the loss of wild-type TP53 through loss of heterozygosity (LOH) is widely found in cancer cells. However, malignant progression induced by cooperation of TP53 GOF mutation and LOH remains poorly understood. Here, we show that mouse intestinal tumors carrying Trp53 GOF mutation with LOH (AKTP
Identifiants
pubmed: 32393735
doi: 10.1038/s41467-020-16245-1
pii: 10.1038/s41467-020-16245-1
pmc: PMC7214469
doi:
Substances chimiques
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2333Références
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