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全反式维甲酸诱导急性早幼粒细胞白血病中CD52的表达。

All-trans-retinoic acid induces CD52 expression in acute promyelocytic leukemia.

作者信息

Li Shi-Wu, Tang Dongqi, Ahrens Kim P, She Jin-Xiong, Braylan Raul C, Yang Lijun

机构信息

Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL 32610, USA.

出版信息

Blood. 2003 Mar 1;101(5):1977-80. doi: 10.1182/blood-2002-05-1426. Epub 2002 Oct 17.

Abstract

It is well known that all-trans-retinoic acid (ATRA) can induce myeloid cell differentiation in acute promyelocytic leukemia (APL) cells. In this study, we found that ATRA treatment of the APL cell line NB4 induced the expression of CD52, both at transcriptional and translational levels. CD52 is a 21- to 28-kDa nonmodulating cell surface glycosylphosphatidylinositol-linked glycoprotein expressed on lymphocytes and monocytes, but not in human myeloid cells. The ATRA-dependent induction of CD52 expression was not observed in non-promyelocytic leukemia cell lines such as K562, U937, and HL-60, suggesting that induction of CD52 by ATRA may be specific to leukemic cells that express promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) or are at the promyelocytic stage of myeloid development. Antibodies against CD52 are used therapeutically against lymphocytes in certain leukemias and in patients undergoing transplantation. An ATRA-induced high level of CD52 expression might potentially serve as a novel therapeutic target in treatment of APL.

摘要

众所周知,全反式维甲酸(ATRA)可诱导急性早幼粒细胞白血病(APL)细胞中的髓样细胞分化。在本研究中,我们发现用ATRA处理APL细胞系NB4可在转录和翻译水平上诱导CD52的表达。CD52是一种21至28 kDa的非调节性细胞表面糖基磷脂酰肌醇连接糖蛋白,在淋巴细胞和单核细胞上表达,但在人髓样细胞中不表达。在非早幼粒细胞白血病细胞系如K562、U937和HL-60中未观察到ATRA依赖性的CD52表达诱导,这表明ATRA诱导CD52可能对表达早幼粒细胞白血病-维甲酸受体α(PML-RARα)或处于髓样发育早幼粒细胞阶段的白血病细胞具有特异性。抗CD52抗体在某些白血病和移植患者中用于治疗淋巴细胞。ATRA诱导的高水平CD52表达可能潜在地成为治疗APL的新治疗靶点。

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