Leveraging increased cytoplasmic nucleoside kinase activity to target mtDNA and oxidative phosphorylation in AML-Reference-Cited by-同舟云学术

Leveraging increased cytoplasmic nucleoside kinase activity to target mtDNA and oxidative phosphorylation in AML

Published:2017-05-11 Issue:19 Volume:129 Page:2657-2666
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Liyanage Sanduni U.¹²,Hurren Rose¹,Voisin Veronique³,Bridon Gaëlle⁴,Wang Xiaoming¹,Xu ChangJiang³,MacLean Neil¹,Siriwardena Thirushi P.²,Gronda Marcela¹,Yehudai Dana¹,Sriskanthadevan Shrivani¹,Avizonis Daina⁴,Shamas-Din Aisha¹,Minden Mark D.¹,Bader Gary D.³,Laposa Rebecca⁵,Schimmer Aaron D.¹

Affiliation:

1. Princess Margaret Cancer Centre, Toronto, ON, Canada;

2. Department of Medical Biophysics, Faculty of Medicine, University of Toronto, Toronto, ON, Canada;

3. Donnelly Centre for Cellular and Biomolecular Research, Toronto, ON, Canada;

4. Goodman Cancer Research Centre, Metabolomics Core Facility, McGill University, Montreal, QC, Canada; and

5. Department of Pharmacology and Toxicology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada

Abstract

Key Points AML cells have increased cytoplasmic nucleoside kinase expression, which functionally contribute to mtDNA biosynthesis. AML cells preferentially activated the nucleoside analog ddC, which inhibited mtDNA replication, oxphos, and induced anti-AML effects.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/129/19/2657/1400312/blood741207.pdf

Reference41 articles.

1. BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells;Lagadinou;Cell Stem Cell,2013

2. Inhibition of mitochondrial translation as a therapeutic strategy for human acute myeloid leukemia;Škrtić;Cancer Cell,2011

3. AML cells have low spare reserve capacity in their respiratory chain that renders them susceptible to oxidative metabolic stress;Sriskanthadevan;Blood,2015

4. Mitochondria: in sickness and in health;Nunnari;Cell,2012

5. Defects in mitochondrial DNA replication and human disease;Copeland;Crit Rev Biochem Mol Biol,2012

Cited by 61 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Deregulation of mitochondrial gene expression in cancer: mechanisms and therapeutic opportunities;British Journal of Cancer;2024-08-14

2. Our current understanding of the biological impact of endometrial cancer mtDNA genome mutations and their potential use as a biomarker;Frontiers in Oncology;2024-06-27

3. Unveiling aging dynamics in the hematopoietic system insights from single-cell technologies;Briefings in Functional Genomics;2024-04-30

4. MYC-driven increases in mitochondrial DNA copy number occur early and persist throughout prostatic cancer progression;JCI Insight;2023-12-22

5. Inhibition of mitochondria induces apoptosis and reduces telomere length and activity in acute myeloid leukemia stem cells;Cell Biochemistry and Function;2023-11-28