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Loss of ISWI ATPase SMARCA5 (SNF2H) in Acute Myeloid Leukemia Cells Inhibits Proliferation and Chromatid Cohesion

T. Zikmund, H. Paszekova, J. Kokavec, P. Kerbs, S. Thakur, T. Turkova, P. Tauchmanova, PA. Greif, T. Stopka,

. 2020 ; 21 (6) : . [pub] 20200318

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc20028374

Grantová podpora
18-01687S, 19-03586S Grantová Agentura České Republiky
GAUK 228316, SVV 260374/2017, UNCE/MED/016, Progres Q26 Univerzita Karlova v Praze
NV19-08-00144 Agentura Pro Zdravotnický Výzkum České Republiky
LM2015040, NPU II LQ1604 (MEYS), OP RDI CZ.1.05/2.1.00/19.0395, CZ.1.05/1.1.00/02.0109 (ERDF, MEYS) Ministerstvo Školství, Mládeže a Tělovýchovy

ISWI chromatin remodeling ATPase SMARCA5 (SNF2H) is a well-known factor for its role in regulation of DNA access via nucleosome sliding and assembly. SMARCA5 transcriptionally inhibits the myeloid master regulator PU.1. Upregulation of SMARCA5 was previously observed in CD34+ hematopoietic progenitors of acute myeloid leukemia (AML) patients. Since high levels of SMARCA5 are necessary for intensive cell proliferation and cell cycle progression of developing hematopoietic stem and progenitor cells in mice, we reasoned that removal of SMARCA5 enzymatic activity could affect the cycling or undifferentiated state of leukemic progenitor-like clones. Indeed, we observed that CRISPR/cas9-mediated SMARCA5 knockout in AML cell lines (S5KO) inhibited the cell cycle progression. We also observed that the SMARCA5 deletion induced karyorrhexis and nuclear budding as well as increased the ploidy, indicating its role in mitotic division of AML cells. The cytogenetic analysis of S5KO cells revealed the premature chromatid separation. We conclude that deleting SMARCA5 in AML blocks leukemic proliferation and chromatid cohesion.

Citace poskytuje Crossref.org

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