Aberrant expression of CKLF-like MARVEL transmembrane member 5 (CMTM5) by promoter methylation in myeloid leukemia
Aberrant expression of CKLF-like MARVEL transmembrane member 5 (CMTM5) by promoter methylation in myeloid leukemia
复制标题
DOI：
10.1016/j.leukres.2010.11.023
复制
发表时间：
2011-06-01
影响因子：
2.7
通讯作者：
Ruan, Guorui
中科院分区：
文献类型：
--
作者：
Niu, Jihong;Li, Henan;Ruan, Guorui
CMTM 5已显示出肿瘤抑制活性，然而，其在白血病中的作用尚不清楚。本文首次报道了CMTM 5在髓系白血病中的表达及功能。CMTM 5在白血病细胞系和白血病患者的骨髓细胞中表达下调或检测不到。CMTM 5-v1的异位表达可明显抑制K562和MEG-01细胞的增殖。此外，CMTM 5与三个白血病特异性融合基因（AML 1-ETO、PML-RAR α和BCR/ABL 1）之间观察到显著负相关。CMTM 5表达在接受治疗的患者中上调。因此，CMTM 5可能参与了髓系白血病的病理机制。(C)2010爱思唯尔有限公司保留所有权利。
CMTM5 has been shown to exhibit tumor suppressor activities, however, its role in leukemia is unclear. Herein we firstly reported the expression and function of CMTM5 in myeloid leukemia. CMTM5 was down-regulated, or undetectable, in leukemia cell lines and bone marrow cells from leukemia patients with promoter methylation. Ectopic expression of CMTM5-v1 strongly inhibited the proliferation of K562 and MEG-01 cells. In addition, significant negative correlations were observed between CMTM5 and three leukemia-specific fusion genes (AML1-ETO, PML-RAR alpha and BCR/ABL1). CMTM5 expression was up-regulated in patients who had undergone treatment. Therefore, CMTM5 may be involved in the pathomechanism of myeloid leukemias. (C) 2010 Elsevier Ltd. All rights reserved.