Graff J R, Greenberg V E, Herman J G, Westra W H, Boghaert E R, Ain K B, Saji M, Zeiger M A, Zimmer S G, Baylin S B
The Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
Cancer Res. 1998 May 15;58(10):2063-6.
Expression of the invasion/metastasis suppressor, E-cadherin, is diminished or lost in thyroid carcinomas. Yet, mutational inactivation of E-cadherin is rare. Herein, we show that this loss is associated with hypermethylation of the E-cadherin 5' CpG island in a panel of human thyroid cancer cell lines. This aberrant methylation is evident in 83% of papillary thyroid carcinoma, 11% of follicular thyroid carcinoma, 40% of Hurthle's cell carcinoma, and 21% of poorly differentiated thyroid carcinomas. Contrary to previous reports, the majority of these poorly differentiated thyroid carcinomas express E-cadherin, but often within the cytoplasm rather than at the cell surface. Together, our data indicate that the invasion/metastasis suppressor function of E-cadherin is frequently compromised in human papillary, Hurthle's cell, and poorly differentiated thyroid carcinoma by epigenetic and biochemical events.
侵袭/转移抑制因子E-钙黏蛋白在甲状腺癌中的表达减少或缺失。然而，E-钙黏蛋白的突变失活很少见。在此，我们表明，在一组人甲状腺癌细胞系中，这种缺失与E-钙黏蛋白5' CpG岛的高甲基化有关。这种异常甲基化在83%的乳头状甲状腺癌、11%的滤泡状甲状腺癌、40%的许特耳氏细胞癌和21%的低分化甲状腺癌中很明显。与之前的报道相反，这些低分化甲状腺癌中的大多数表达E-钙黏蛋白，但通常在细胞质内而不是细胞表面。总之，我们的数据表明，在人乳头状、许特耳氏细胞和低分化甲状腺癌中，E-钙黏蛋白的侵袭/转移抑制功能经常因表观遗传和生化事件而受损。
