Author
Listed:
- Bin Zhang
(City of Hope Medical Center and Beckman Research Institute)
- Dandan Zhao
(City of Hope Medical Center and Beckman Research Institute)
- Fang Chen
(City of Hope Medical Center and Beckman Research Institute)
- David Frankhouser
(City of Hope Medical Center and Beckman Research Institute)
- Huafeng Wang
(City of Hope Medical Center and Beckman Research Institute
Zhejiang University)
- Khyatiben V. Pathak
(Cancer & Cell Biology Division, Translational Genomics Research Institute
City of Hope Comprehensive Cancer Center)
- Lei Dong
(Beckman Research Institute of City of Hope)
- Anakaren Torres
(Cancer & Cell Biology Division, Translational Genomics Research Institute
City of Hope Comprehensive Cancer Center)
- Krystine Garcia-Mansfield
(Cancer & Cell Biology Division, Translational Genomics Research Institute
City of Hope Comprehensive Cancer Center)
- Yi Zhang
(City of Hope Medical Center and Beckman Research Institute
Zhejiang University)
- Dinh Hoa Hoang
(City of Hope Medical Center and Beckman Research Institute)
- Min-Hsuan Chen
(City of Hope National Medical Center, Integrative Genomics Core, Department of Computational and Quantitative Medicine, Beckman Research Institute)
- Shu Tao
(City of Hope National Medical Center, Integrative Genomics Core, Department of Computational and Quantitative Medicine, Beckman Research Institute)
- Hyejin Cho
(City of Hope National Medical Center, Integrative Genomics Core, Department of Computational and Quantitative Medicine, Beckman Research Institute)
- Yong Liang
(DNA/RNA Peptide Shared Resources, Beckman Research Institute)
- Danilo Perrotti
(University of Maryland School of Medicine Baltimore
Centre of Hematology, Imperial College of London)
- Sergio Branciamore
(City of Hope Medical Center and Beckman Research Institute)
- Russell Rockne
(City of Hope Medical Center and Beckman Research Institute)
- Xiwei Wu
(City of Hope National Medical Center, Integrative Genomics Core, Department of Computational and Quantitative Medicine, Beckman Research Institute)
- Lucy Ghoda
(City of Hope Medical Center and Beckman Research Institute)
- Ling Li
(City of Hope Medical Center and Beckman Research Institute)
- Jie Jin
(Zhejiang University)
- Jianjun Chen
(Beckman Research Institute of City of Hope)
- Jianhua Yu
(City of Hope National Medical Center)
- Michael A. Caligiuri
(City of Hope National Medical Center)
- Ya-Huei Kuo
(City of Hope Medical Center and Beckman Research Institute)
- Mark Boldin
(Beckman Research Institute of City of Hope)
- Rui Su
(Beckman Research Institute of City of Hope)
- Piotr Swiderski
(DNA/RNA Peptide Shared Resources, Beckman Research Institute)
- Marcin Kortylewski
(Beckman Research Institute)
- Patrick Pirrotte
(Cancer & Cell Biology Division, Translational Genomics Research Institute
City of Hope Comprehensive Cancer Center)
- Le Xuan Truong Nguyen
(City of Hope Medical Center and Beckman Research Institute
Cancer & Cell Biology Division, Translational Genomics Research Institute)
- Guido Marcucci
(City of Hope Medical Center and Beckman Research Institute)
Abstract
The mechanisms underlying the transformation of chronic myeloid leukemia (CML) from chronic phase (CP) to blast crisis (BC) are not fully elucidated. Here, we show lower levels of miR-142 in CD34+CD38− blasts from BC CML patients than in those from CP CML patients, suggesting that miR-142 deficit is implicated in BC evolution. Thus, we create miR-142 knockout CML (i.e., miR-142−/−BCR-ABL) mice, which develop BC and die sooner than miR-142 wt CML (i.e., miR-142+/+BCR-ABL) mice, which instead remain in CP CML. Leukemic stem cells (LSCs) from miR-142−/−BCR-ABL mice recapitulate the BC phenotype in congenic recipients, supporting LSC transformation by miR-142 deficit. State-transition and mutual information analyses of “bulk” and single cell RNA-seq data, metabolomic profiling and functional metabolic assays identify enhanced fatty acid β-oxidation, oxidative phosphorylation and mitochondrial fusion in LSCs as key steps in miR-142-driven BC evolution. A synthetic CpG-miR-142 mimic oligodeoxynucleotide rescues the BC phenotype in miR-142−/−BCR-ABL mice and patient-derived xenografts.
Suggested Citation
Bin Zhang & Dandan Zhao & Fang Chen & David Frankhouser & Huafeng Wang & Khyatiben V. Pathak & Lei Dong & Anakaren Torres & Krystine Garcia-Mansfield & Yi Zhang & Dinh Hoa Hoang & Min-Hsuan Chen & Shu, 2023.
"Acquired miR-142 deficit in leukemic stem cells suffices to drive chronic myeloid leukemia into blast crisis,"
Nature Communications, Nature, vol. 14(1), pages 1-21, December.
Handle:
RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-41167-z
DOI: 10.1038/s41467-023-41167-z
Download full text from publisher
References listed on IDEAS
- Koichi Akashi & David Traver & Toshihiro Miyamoto & Irving L. Weissman, 2000.
"A clonogenic common myeloid progenitor that gives rise to all myeloid lineages,"
Nature, Nature, vol. 404(6774), pages 193-197, March.
- Shan Wang & Ning Li & Maryam Yousefi & Angela Nakauka-Ddamba & Fan Li & Kimberly Parada & Shilpa Rao & Gerard Minuesa & Yarden Katz & Brian D. Gregory & Michael G. Kharas & Zhengquan Yu & Christopher , 2015.
"Transformation of the intestinal epithelium by the MSI2 RNA-binding protein,"
Nature Communications, Nature, vol. 6(1), pages 1-15, May.
Full references (including those not matched with items on IDEAS)
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