Increasing TET Expression and 5‐Hydroxymethylcytosine Formation by a Carbocyclic 5‐Aza‐2′‐deoxy‐cytidine Antimetabolite

M Maike Däther (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) E Elsa Peev (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) A Annika Fröhlich (Research Unit Apoptosis in Hematopoietic Stem Cells Helmholtz Munich German Research Center for Environmental Health (HMGU) Munich Germany) B Binje Vick S Sogol Fatourechi (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) G Gilles Gasparoni M Matthias Heiß C Corinna C. Pleintinger (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) E Emmanuel Asu Bisong (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) H Hans Hurmiz (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) D Davide Guglielminotti (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) Y Yasmin V. Gärtner (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) T Tina Aumer (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) K Karsten Spiekermann (Ludwig Maximilian University Hospital, Munich, Germany) J Jörn Walter I Irmela Jeremias F Franziska R. Traube (Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany) T Thomas Carell

Abstract

ABSTRACT Ten‐eleven translocation (TET) enzymes are critical epigenetic regulators, which oxidize the methylated cytosine nucleobase 5‐methyl‐dC (mdC) in the genome to 5‐hydroxymethyl‐dC (hmdC) in an α‐ketoglutarate‐dependent manner. Because the presence of mdC in the promoter region of a given gene silences its expression, this oxidation goes in hand with the reactivation of such silenced genes. In different highly aggressive cancers such as acute myeloid leukemia (AML) and glioblastoma, loss of TET enzyme function, and therefore reduced hmdC levels pave the way for tumor development. Impairment of TET activity can occur through metabolic inhibition, through loss‐of‐function mutations in TET genes themselves, and finally through suppression of TET‐expression via epigenetic silencing. Reactivation of TET enzyme expression represents a major aim of epigenetic cancer therapy. Here we show that the carbocyclic antimetabolite 5‐aza‐2′deoxycytidine (cAzadC), which is supposed to suppress the methylation of DNA during replication, leads to a substantial increase of TET2 expression and strongly increasing hmdC levels. We show that the treatment with cAzadC goes in hand with the broad reactivation of the cellular antitumor responses. With patient‐derived xenograft AML‐mouse models, we show that this translates into a strongly improved anticancer effect in vivo.

Article Details

Volume / Issue Vol. 65, Issue 32
Published August 03, 2026
ISSN 1433-7851
Publisher Wiley

Journal Info

Angewandte Chemie International Edition

Wiley

ISSN: 1433-7851 Physical Sciences

Authors (18)

M

Maike Däther

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

E

Elsa Peev

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

A

Annika Fröhlich

Research Unit Apoptosis in Hematopoietic Stem Cells Helmholtz Munich German Research Center for Environmental Health (HMGU) Munich Germany

B

Binje Vick

S

Sogol Fatourechi

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

G

Gilles Gasparoni

M

Matthias Heiß

C

Corinna C. Pleintinger

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

E

Emmanuel Asu Bisong

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

H

Hans Hurmiz

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

D

Davide Guglielminotti

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

Y

Yasmin V. Gärtner

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

T

Tina Aumer

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

K

Karsten Spiekermann

Ludwig Maximilian University Hospital, Munich, Germany

J

Jörn Walter

I

Irmela Jeremias

F

Franziska R. Traube

Institute for Chemical Epigenetics and Center for Nucleic Acid Therapies Department of Chemistry LMU Munich Munich Germany

T

Thomas Carell