Increased Genetic Instability and Accelerated Progression of Colitis-Associated Colorectal Cancer through Intestinal Epithelium-specific Deletion of
Animals
Carcinogenesis
Cell Proliferation
/ physiology
Centrosome
/ metabolism
Colitis
/ genetics
Colorectal Neoplasms
/ genetics
Gene Deletion
Intestinal Mucosa
/ metabolism
Kruppel-Like Factor 4
Kruppel-Like Transcription Factors
/ deficiency
MAP Kinase Signaling System
Mice
Tumor Suppressor Protein p53
/ genetics
Journal
Molecular cancer research : MCR
ISSN: 1557-3125
Titre abrégé: Mol Cancer Res
Pays: United States
ID NLM: 101150042
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
22
04
2018
revised:
05
07
2018
accepted:
08
08
2018
pubmed:
16
8
2018
medline:
24
1
2020
entrez:
16
8
2018
Statut:
ppublish
Résumé
Krüppel-like factor 4 (KLF4), a zinc finger transcription factor, regulates homeostasis of the intestinal epithelium. Previously, it was reported that KLF4 functions as a tumor suppressor in colorectal cancer. Here, evidence demonstrates that KLF4 mitigates the development and progression of colitis-associated colorectal cancer (CAC) in a murine model. Mice with intestinal epithelium-specific deletion of
Identifiants
pubmed: 30108164
pii: 1541-7786.MCR-18-0399
doi: 10.1158/1541-7786.MCR-18-0399
pmc: PMC6318049
mid: NIHMS1503910
doi:
Substances chimiques
Klf4 protein, mouse
0
Kruppel-Like Factor 4
0
Kruppel-Like Transcription Factors
0
Trp53 protein, mouse
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
165-176Subventions
Organisme : NCI NIH HHS
ID : R01 CA084197
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK052230
Pays : United States
Informations de copyright
©2018 American Association for Cancer Research.
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