Overexpression of murine fizzy-related (fzr) increases natural killer cell-mediated cell death and suppresses tumor growth
Overexpression of murine fizzy-related (fzr) increases natural killer cell-mediated cell death and suppresses tumor growth
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DOI：
10.1182/blood.v96.1.259.013k36_259_263
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发表时间：
2000-07-01
期刊：
影响因子：
20.3
通讯作者：
Braun, J
中科院分区：
文献类型：
--
作者：
Wang, CX;Fisk, BC;Braun, J
Fizzy-related （fzr）是最近发现的一个参与果蝇和酵母细胞周期调控的7WD结构域家族成员。在这项研究中，fzr的小鼠同源基因通过抑制减法杂交被分离出来，作为在小鼠b淋巴瘤细胞系恶性进展过程中表达降低的基因。b -淋巴瘤细胞中fzr逆转录病毒的过表达可减少肿瘤的形成。那些出现的肿瘤已经减少或消灭了逆转录病毒Fzr。令人惊讶的是，fzr过表达显著增加了b淋巴瘤细胞对自然杀伤细胞（NK）细胞毒性的易感性，这是该模型系统中肿瘤形成的宿主抗性机制。这些发现提示fzr是一类抑制b细胞肿瘤发生的新基因，并提示fzr在靶细胞与NK细胞相互作用中的新作用。（Blood. 2000;96:259-263） (C) 1990年由美国血液学会出版。
Fizzy-related (fzr) is a recently identified 7WD domain family member implicated in cell cycle regulation of Drosophila and yeast. In this study the murine homologue of fzr was isolated by suppression subtractive hybridization as a gene with decreased expression during malignant progression of a murine B-lymphoma cell line. Retroviral overexpression of fzr in B-lymphoma cells reduced tumor formation. Those tumors that did arise had diminished or extinguished retroviral Fzr. Surprisingly, fzr overexpression dramatically increased B-lymphoma cell susceptibility to natural killer cell (NK) cytotoxicity, a host-resistant mechanism for tumor formation in this model system. These findings implicate fzr as a new category of genes suppressing B-cell tumorigenesis and suggest a novel role for fzr in the target cell interaction with NK cells. (Blood. 2000;96:259-263) (C) 2090 by The American Society of Hematology.