Overexpression of a cell adhesion molecule, TSLC1, as a possible molecular marker for acute-type adult T-cell leukemia
Overexpression of a cell adhesion molecule, TSLC1, as a possible molecular marker for acute-type adult T-cell leukemia
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DOI：
10.1182/blood-2004-03-1222
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发表时间：
2005-02-01
期刊：
影响因子：
20.3
通讯作者：
Morishita, K
中科院分区：
文献类型：
--
作者：
Sasaki, H;Nishikata, I;Morishita, K
成人t细胞白血病（ATL）是由人类t细胞白血病病毒1型（HTLV-1）感染引起的，在HTLV-1携带者中发生率为2% ~ 4%，潜伏期长，提示ATL的发生有额外的改变参与。为了表征和鉴定ATL的新标志物，我们使用微阵列检测了8例急性ATL中超过12000个基因的表达谱。与CD4（+）和CD4(+)CD45RO(+) T细胞相比，含有白细胞介素2 （IL-2）受体α的192个基因表达上调2倍以上，肺癌肿瘤抑制因子1 （TSLC1）、caveolin 1、前列腺素D2合成酶表达上调30倍以上。TSLC1是一种细胞粘附分子，最初在肺中被鉴定为肿瘤抑制因子，但在正常或活化的T细胞中缺乏表达。我们证实TSLC1在所有急性ATL细胞和10个ATL或HTLV-1感染t细胞系中的7个中异位表达。将TSLC1导入人ATL细胞系ED，增强了其对血管内皮细胞的自聚集和粘附能力。这些结果提示，TSLC1的异位表达可能为急性ATL提供新的标志物，并可能参与组织侵袭，这是恶性ATL细胞的一个特征。(C) 2005年由美国血液病学会出版。
Adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1) infection, occurs in 2% to 4% of the HTLV-1 carriers with a long latent period, suggesting that additional alterations participate in the development of ATL. To characterize and identify novel markers of ATL, we examined the expression profiles of more than 12 000 genes in 8 cases of acute-type ATL using microarray. One hundred ninety-two genes containing interleukin 2 (IL-2) receptor alpha were up-regulated more than 2-fold compared with CD4(+) and CD4(+)CD45RO(+) T cells, and tumor suppressor in lung cancer 1 (TSLC1), caveolin 1, and prostaglandin D2 synthase showed increased expression of more than 30-fold. TSLC1 is a cell adhesion molecule originally identified as a tumor suppressor in the lung but lacks its expression in normal or activated T cells. We confirmed ectopic expression of the TSLC1 in all acute-type ATL cells and in 7 of 10 ATL- or HTLV-1 infected T-cell lines. Introduction of TSLC1 into a human ATL cell line ED enhanced both self-aggregation and adhesion ability to vascular endothelial cells. These results suggested that the ectopic expression of TSLC1 could provide a novel marker for acute-type ATL and may participate in tissue invasion, a characteristic feature of the malignant ATL cells. (C) 2005 by The American Society of Hematology.