Chromatin remodeling gene SMARCA5 is dysregulated in primitive hematopoietic cells of acute leukemia
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Leukemia, Erythroblastic, Acute genetics metabolism pathology MeSH
- Acute Disease MeSH
- Cell Differentiation drug effects genetics MeSH
- Chromatin metabolism MeSH
- DNA Topoisomerases, Type II biosynthesis genetics MeSH
- Erythroid Precursor Cells metabolism pathology MeSH
- Phenylhydrazines toxicity MeSH
- Hematopoietic Stem Cells metabolism pathology MeSH
- Hematopoiesis genetics MeSH
- Anemia, Hemolytic chemically induced metabolism pathology MeSH
- Bone Marrow metabolism pathology MeSH
- Humans MeSH
- RNA, Messenger biosynthesis MeSH
- Leukemia, Myeloid genetics metabolism pathology MeSH
- Mice, Inbred C3H MeSH
- Mice MeSH
- Tumor Cells, Cultured MeSH
- Neoplastic Stem Cells metabolism pathology MeSH
- Neoplasm Proteins biosynthesis genetics MeSH
- High Mobility Group Proteins biosynthesis genetics MeSH
- Gene Expression Regulation, Leukemic * MeSH
- RNA, Neoplasm biosynthesis MeSH
- Spleen metabolism pathology MeSH
- Gene Expression Profiling MeSH
- Subtraction Technique MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chromatin MeSH
- DNA Topoisomerases, Type II MeSH
- Phenylhydrazines MeSH
- RNA, Messenger MeSH
- Neoplasm Proteins MeSH
- phenylhydrazine MeSH Browser
- High Mobility Group Proteins MeSH
- RNA, Neoplasm MeSH
We identified a subset of genes involved in chromatin remodeling whose mRNA expression changes in differentiating mouse erythroleukemia (MEL) cells. We furthermore tested their mRNA expression patterns in normal and malignant CD34+ bone marrow cells. SMARCA5, imitation switch gene homologue, was rapidly silenced during in vitro erythroid differentiation of MEL cells whereas it was up-regulated in CD34+ hematopoietic progenitors of acute myeloid leukemia (AML) patients. Moreover, SMARCA5 mRNA levels decreased in AML CD34+ progenitors after the patients achieved complete hematologic remission. We detected high levels of SMARCA5 mRNA in murine bone marrow and spleen and monitored its expression in these hematopoietic tissues during accelerated hematopoiesis following hemolytic anemia induced by phenylhydrazine. SMARCA5 expression levels decreased after the onset of accelerated erythropoiesis. Our data suggest that both in vitro and in vivo induction of differentiation is followed by down-regulation of SMARCA5 expression. In CD34+ AML progenitors over-expression of SMARCA5 may thus dysregulate the genetic program required for normal differentiation.
References provided by Crossref.org
SMARCA5-mediated chromatin remodeling is required for germinal center formation
Epigenetic control of SPI1 gene by CTCF and ISWI ATPase SMARCA5
Nuclear localization of ISWI ATPase Smarca5 (Snf2h) in mouse
