犬类淋巴肿瘤细胞中通过启动子高甲基化对p16肿瘤抑制基因表达的抑制作用。
Inhibition of p16 tumor suppressor gene expression via promoter hypermethylation in canine lymphoid tumor cells.
作者信息
Fujiwara-Igarashi Aki, Goto-Koshino Yuko, Mochizuki Hiroyuki, Sato Masahiko, Fujino Yasuhito, Ohno Koichi, Tsujimoto Hajime
机构信息
Department of Veterinary Internal Medicine, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.
Department of Veterinary Internal Medicine, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.
出版信息
Res Vet Sci. 2014 Aug;97(1):60-3. doi: 10.1016/j.rvsc.2014.04.008. Epub 2014 Apr 24.
To investigate the epigenetic regulation of the p16 gene in canine lymphoid tumor cells, its methylation status was examined in four canine lymphoid tumor cell lines. In three canine lymphoid tumor cell lines (CLBL-1, GL-1, and UL-1) with low-level p16 mRNA expression, 20 CpG sites in the promoter region of p16 gene were consistently methylated although all of the CpG sites were not methylated in another cell line (CL-1) and normal lymph node cells. The expression level of p16 mRNA in these three cell lines was restored after cultivation in the presence of a methylation inhibitor, 5-Aza-2'-deoxycitidine, indicating inactivation of p16 gene via hypermethylation. This study revealed the inactivation of p16 gene through hypermethylation of its CpG island in a fraction of canine lymphoid tumor cells.
为研究犬类淋巴瘤细胞中p16基因的表观遗传调控，检测了四种犬类淋巴瘤细胞系中该基因的甲基化状态。在三个p16 mRNA表达水平较低的犬类淋巴瘤细胞系（CLBL-1、GL-1和UL-1）中，p16基因启动子区域的20个CpG位点持续发生甲基化，尽管在另一个细胞系（CL-1）和正常淋巴结细胞中并非所有CpG位点都发生甲基化。在甲基化抑制剂5-氮杂-2'-脱氧胞苷存在的情况下培养后，这三个细胞系中p16 mRNA的表达水平得以恢复，表明p16基因通过高甲基化而失活。本研究揭示了部分犬类淋巴瘤细胞中p16基因的CpG岛通过高甲基化而失活。
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