Glud Sys Zoffmann, Sørensen Annette Balle, Andrulis Mindaugas, Wang Bruce, Kondo Eisaku, Jessen Randi, Krenacs Laszlo, Stelkovics Eva, Wabl Matthias, Serfling Edgar, Palmetshofer Alois, Pedersen Finn Skou
Department of Molecular Biology, University of Aarhus, Denmark.
Blood. 2005 Nov 15;106(10):3546-52. doi: 10.1182/blood-2005-02-0493. Epub 2005 Jul 28.
Nuclear factor of activated T cell (NFAT) transcription factors play a central role in differentiation, activation, and elimination of lymphocytes. We here report on the finding of provirus integration into the Nfatc3 locus in T-cell lymphomas induced by the murine lymphomagenic retrovirus SL3-3 and show that NFATc3 expression is repressed in these lymphomas. The provirus insertions are positioned close to the Nfatc3 promoter or a putative polyadenylated RNA (polyA) region. Furthermore, we demonstrate that NFATc3-deficient mice infected with SL3-3 develop T-cell lymphomas faster and with higher frequencies than wild-type mice or NFATc2-deficient mice. These results identify NFATc3 as a tumor suppressor for the development of murine T-cell lymphomas induced by the retrovirus SL3-3.
活化T细胞核因子(NFAT)转录因子在淋巴细胞的分化、激活和清除过程中发挥核心作用。我们在此报告了在小鼠淋巴瘤逆转录病毒SL3-3诱导的T细胞淋巴瘤中,前病毒整合到Nfatc3基因座的发现,并表明在这些淋巴瘤中NFATc3的表达受到抑制。前病毒插入位点靠近Nfatc3启动子或一个假定的多聚腺苷酸化RNA(polyA)区域。此外,我们证明感染SL3-3的NFATc3缺陷小鼠比野生型小鼠或NFATc2缺陷小鼠更快且更频繁地发生T细胞淋巴瘤。这些结果确定NFATc3是逆转录病毒SL3-3诱导的小鼠T细胞淋巴瘤发生过程中的一种肿瘤抑制因子。