MXD3缺失诱导Reh人前体B急性淋巴细胞白血病细胞凋亡。
Loss of MXD3 induces apoptosis of Reh human precursor B acute lymphoblastic leukemia cells.
作者信息
Barisone Gustavo A, Satake Noriko, Lewis Carly, Duong Connie, Chen Cathy, Lam Kit S, Nolta Jan, Dίaz Elva
机构信息
Department of Pharmacology, UC Davis School of Medicine, Davis, CA, USA.
Department of Pediatrics, Hematology/Oncology Section, UC Davis School of Medicine, Sacramento, CA, USA; Stem Cell Program and Institute of Regenerative Cures, UC Davis School of Medicine, Sacramento, CA, USA.
出版信息
Blood Cells Mol Dis. 2015 Apr;54(4):329-35. doi: 10.1016/j.bcmd.2014.12.002. Epub 2014 Dec 20.
Abstract
MXD3 is a transcription factor that plays an important role in proliferation of human DAOY medulloblastoma cells. Here, we demonstrate that MXD3 is highly enriched in human precursor B acute lymphoblastic leukemia (preB ALL) samples compared to mobilized peripheral blood mononuclear cells, bone marrow, or hematopoietic stem cells from healthy donors. MXD3 knock-down in the preB ALL cell line Reh resulted in decreased cell numbers with no change in G0/G1, S or G2/M populations but increased apoptosis compared to control cells. Our results suggest that MXD3 is important for survival of Reh preB ALL cells, possibly as an anti-apoptotic factor.
摘要
MXD3是一种转录因子，在人类DAOY髓母细胞瘤细胞的增殖中发挥重要作用。在此，我们证明，与健康供体的动员外周血单个核细胞、骨髓或造血干细胞相比，MXD3在人类前体B急性淋巴细胞白血病（preB ALL）样本中高度富集。在preB ALL细胞系Reh中敲低MXD3导致细胞数量减少，G0/G1、S或G2/M期细胞群体无变化，但与对照细胞相比，细胞凋亡增加。我们的结果表明，MXD3对Reh preB ALL细胞的存活很重要，可能作为一种抗凋亡因子。
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