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MLL-AF9– and HOXA9-mediated acute myeloid leukemia stem cell self-renewal requires JMJD1C

by Chu, S. Haihua , Roeder, Robert G. , Rahnamay, Noushin F. , Eng, Rowena , Ebert, Benjamin L. , Xu, Haiming , Sinha, Amit U. , DeJong, Joshua , Koche, Richard , Deshpande, Aniruddha J. , Armstrong, Scott A. , Zhu, Nan , Minehart, Janna C. , Chen, Mo , Al-Shahrour, Fatima , Chen, Chun-Wei

in Animals / Biomedical research / Cancer / Cell Self Renewal / Cellular proteins / Data analysis / Epigenetics / Gene Expression / Genetic aspects / Health aspects / Hematopoietic stem cells / Hematopoietic Stem Cells - physiology / Homeodomain Proteins - physiology / Jumonji Domain-Containing Histone Demethylases - physiology / Leukemia / Leukemia, Myeloid, Acute - genetics / Leukemia, Myeloid, Acute - metabolism / Leukemia, Myeloid, Acute - pathology / Medical prognosis / Mice, Knockout / Neoplasm Transplantation / Neoplastic Stem Cells - physiology / Oncogene Proteins, Fusion - physiology / Proteins / Rodents / Stem cells / Tumor Cells, Cultured

2016

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MLL-AF9– and HOXA9-mediated acute myeloid leukemia stem cell self-renewal requires JMJD1C

2016

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MLL-AF9– and HOXA9-mediated acute myeloid leukemia stem cell self-renewal requires JMJD1C

2016

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Journal Article

MLL-AF9– and HOXA9-mediated acute myeloid leukemia stem cell self-renewal requires JMJD1C

Chu, S. Haihua,

Roeder, Robert G.,

Rahnamay, Noushin F.,

Eng, Rowena,

Ebert, Benjamin L.,

Xu, Haiming,

Sinha, Amit U.,

DeJong, Joshua,

Koche, Richard,

Deshpande, Aniruddha J.,

Armstrong, Scott A.,

Zhu, Nan,

Minehart, Janna C.,

Chen, Mo,

Al-Shahrour, Fatima,

Chen, Chun-Wei

2016

Overview

Self-renewal is a hallmark of both hematopoietic stem cells (HSCs) and leukemia stem cells (LSCs); therefore, the identification of mechanisms that are required for LSC, but not HSC, function could provide therapeutic opportunities that are more effective and less toxic than current treatments. Here, we employed an in vivo shRNA screen and identified jumonji domain-containing protein JMJD1C as an important driver of MLL-AF9 leukemia. Using a conditional mouse model, we showed that loss of JMJD1C substantially decreased LSC frequency and caused differentiation of MLL-AF9- and homeobox A9-driven (HOXA9-driven) leukemias. We determined that JMJD1C directly interacts with HOXA9 and modulates a HOXA9-controlled gene-expression program. In contrast, loss of JMJD1C led to only minor defects in blood homeostasis and modest effects on HSC self-renewal. Together, these data establish JMJD1C as an important mediator of MLL-AF9- and HOXA9-driven LSC function that is largely dispensable for HSC function.

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Publisher

American Society for Clinical Investigation

Subject

Animals

/ Biomedical research

/ Cancer