TET3 promotes AML growth and epigenetically regulates glucose metabolism and leukemic stem cell associated pathways.


Journal

Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895

Informations de publication

Date de publication:
02 2022
Historique:
received: 07 04 2021
accepted: 17 08 2021
revised: 07 08 2021
pubmed: 1 9 2021
medline: 16 2 2022
entrez: 31 8 2021
Statut: ppublish

Résumé

Acute myeloid leukemia (AML) is considered a poor prognosis malignancy where patients exhibit altered glucose metabolism and stem cell signatures that contribute to AML growth and maintenance. Here, we report that the epigenetic factor, Ten-Eleven Translocation 3 (TET3) dioxygenase is overexpressed in AML patients and functionally validated human leukemic stem cells (LSCs), is required for leukemic growth by virtue of its regulation of glucose metabolism in AML cells. In human AML cells, TET3 maintains 5-hydroxymethylcytosine (5hmC) epigenetic marks and expression of early myeloid progenitor program, critical glucose metabolism and STAT5A signaling pathway genes, which also positively correlate with TET3 expression in AML patients. Consequently, TET3 depletion impedes hexokinase activity and L-Lactate production in AML cells. Conversely, overexpression of TET3 in healthy human hematopoietic stem progenitors (HSPCs) upregulates the expression of glucose metabolism, STAT5A signaling and AML associated genes, and impairs normal HSPC lineage differentiation in vitro. Finally, TET3 depletion renders AML cells highly sensitive to blockage of the TET3 downstream pathways glycolysis and STAT5 signaling via the combination of 2-Deoxy-D-glucose and STAT5 inhibitor which preferentially targets AML cells but spares healthy CD34

Identifiants

pubmed: 34462525
doi: 10.1038/s41375-021-01390-3
pii: 10.1038/s41375-021-01390-3
doi:

Substances chimiques

TET3 protein, human EC 1.-
Dioxygenases EC 1.13.11.-
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

416-425

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Alex Jose Pulikkottil (AJ)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Shiva Bamezai (S)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Tobias Ammer (T)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Fabian Mohr (F)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Kristin Feder (K)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Naidu M Vegi (NM)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Tamoghna Mandal (T)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany.

Ursula Kohlhofer (U)

Institute of Pathology, University Hospital Tübingen, Tübingen, Germany.

Leticia Quintanilla-Martinez (L)

Institute of Pathology, University Hospital Tübingen, Tübingen, Germany.

Amit Sinha (A)

Basepair, New York, NY, USA.

Christian Buske (C)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany. christian.buske@uni-ulm.de.

Vijay P S Rawat (VPS)

Institute of Experimental Cancer Research, University Hospital of Ulm, Ulm, Germany. vijaypsrawat@mail.jnu.ac.in.
Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India. vijaypsrawat@mail.jnu.ac.in.

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