Histone H1.2 Represses the Transcription of the
H1.2
INK4 locus
YB-1
p16
transcription
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
received:
15
05
2023
revised:
06
06
2023
accepted:
13
06
2023
medline:
31
7
2023
pubmed:
28
7
2023
entrez:
27
7
2023
Statut:
ppublish
Résumé
CDK inhibitor p16 plays a pivotal role in the induction of cellular senescence and functions as a tumor suppressor. Here, we demonstrate that histone H1.2 is involved in p16 repression. Cells were transfected with siRNAs and subjected to quantitative reverse transcription-polymerase chain reaction, immunoblotting and chromatin immunoprecipitation (ChIP) assay. The decrease in H1.2 by oncogenic RAS was associated with increased levels of p16. Depletion of H1.2 selectively increased p16, but not alternative reading frame (ARF) mRNA. ChIP assay showed that H1.2 directly bound to the p16 promoter. Interestingly, silencing YB-1, a component of H1.2 complex, decreased the expression levels of H1.2, resulting in decreased binding of H1.2 on the p16 promoter. These results provide a model in which H1.2 is positively regulated by YB-1 and directly binds to and represses the transcription of p16.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
CDK inhibitor p16 plays a pivotal role in the induction of cellular senescence and functions as a tumor suppressor. Here, we demonstrate that histone H1.2 is involved in p16 repression.
MATERIALS AND METHODS
METHODS
Cells were transfected with siRNAs and subjected to quantitative reverse transcription-polymerase chain reaction, immunoblotting and chromatin immunoprecipitation (ChIP) assay.
RESULTS
RESULTS
The decrease in H1.2 by oncogenic RAS was associated with increased levels of p16. Depletion of H1.2 selectively increased p16, but not alternative reading frame (ARF) mRNA. ChIP assay showed that H1.2 directly bound to the p16 promoter. Interestingly, silencing YB-1, a component of H1.2 complex, decreased the expression levels of H1.2, resulting in decreased binding of H1.2 on the p16 promoter.
CONCLUSION
CONCLUSIONS
These results provide a model in which H1.2 is positively regulated by YB-1 and directly binds to and represses the transcription of p16.
Identifiants
pubmed: 37500167
pii: 43/8/3441
doi: 10.21873/anticanres.16519
doi:
Substances chimiques
Histones
0
Cyclin-Dependent Kinase Inhibitor p16
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
3441-3446Informations de copyright
Copyright © 2023 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.