Histone chaperone ASF1A accelerates chronic myeloid leukemia blast crisis by activating Notch signaling.
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
03 10 2022
03 10 2022
Historique:
received:
05
05
2022
accepted:
05
09
2022
revised:
29
08
2022
entrez:
2
10
2022
pubmed:
3
10
2022
medline:
5
10
2022
Statut:
epublish
Résumé
The blast crisis (BC) is the final deadly phase of chronic myeloid leukemia (CML), which remains a major challenge in clinical management. However, the underlying molecular mechanism driving blastic transformation remains unclear. Here, we show that ASF1A, an essential activator, enhanced the transformation to CML-BC by mediating cell differentiation arrest. ASF1A expression was aberrantly increased in bone marrow samples from CML-BC patients compared with newly diagnosed CML-chronic phase (CP) patients. ASF1A inhibited cell differentiation and promoted CML development in vivo. Mechanistically, we identified ASF1A as a coactivator of the Notch transcriptional complex that induces H3K56ac modification in the promoter regions of Notch target genes, and subsequently enhanced RBPJ binding to these promoter regions, thereby enhancing Notch signaling activation to mediate differentiation arrest in CML cells. Thus, our work suggests that targeting ASF1A might represent a promising therapeutic approach and a biomarker to detect disease progression in CML patients.
Identifiants
pubmed: 36184659
doi: 10.1038/s41419-022-05234-5
pii: 10.1038/s41419-022-05234-5
pmc: PMC9527247
doi:
Substances chimiques
ASF1A protein, human
0
Cell Cycle Proteins
0
Histone Chaperones
0
Molecular Chaperones
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
842Informations de copyright
© 2022. The Author(s).
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