Acute myeloid leukemia induces protumoral p16INK4a-driven senescence in the bone marrow microenvironment.
Animals
Bone Marrow
/ metabolism
Cell Proliferation
Cellular Senescence
Coculture Techniques
Cyclin-Dependent Kinase Inhibitor p16
/ metabolism
Female
Humans
Leukemia, Myeloid, Acute
/ metabolism
Mesenchymal Stem Cells
/ metabolism
Mice, Inbred C57BL
NADPH Oxidase 2
/ metabolism
Superoxides
/ metabolism
Tumor Cells, Cultured
Tumor Microenvironment
Journal
Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509
Informations de publication
Date de publication:
31 01 2019
31 01 2019
Historique:
received:
14
04
2018
accepted:
31
10
2018
pubmed:
8
11
2018
medline:
8
10
2019
entrez:
8
11
2018
Statut:
ppublish
Résumé
Acute myeloid leukemia (AML) is an age-related disease that is highly dependent on the bone marrow (BM) microenvironment. With increasing age, tissues accumulate senescent cells, characterized by an irreversible arrest of cell proliferation and the secretion of a set of proinflammatory cytokines, chemokines, and growth factors, collectively known as the senescence-associated secretory phenotype (SASP). Here, we report that AML blasts induce a senescent phenotype in the stromal cells within the BM microenvironment and that the BM stromal cell senescence is driven by p16INK4a expression. The p16INK4a-expressing senescent stromal cells then feed back to promote AML blast survival and proliferation via the SASP. Importantly, selective elimination of p16INK4a
Identifiants
pubmed: 30401703
pii: S0006-4971(20)42832-0
doi: 10.1182/blood-2018-04-845420
pmc: PMC6356984
doi:
Substances chimiques
Cyclin-Dependent Kinase Inhibitor p16
0
Superoxides
11062-77-4
NADPH Oxidase 2
EC 1.6.3.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
446-456Références
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