Aberrant glycosylation of E-cadherin enhances cell-cell binding to suppress metastasis
Aberrant glycosylation of E-cadherin enhances cell-cell binding to suppress metastasis
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DOI：
10.1074/jbc.271.23.13811
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发表时间：
1996-06-07
影响因子：
4.8
通讯作者：
Taniguchi, N
中科院分区：
文献类型：
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作者：
Yoshimura, M;Ihara, Y;Taniguchi, N
据报道，β 1-4 N-乙酰葡糖胺基转移酶（GnT-III）基因的引入抑制了高转移性B16-hm鼠黑素瘤细胞中的转移（Yoshimura，M.，Nishikawa，A.，Ihara，Y.，Taniguchi，S.，和Taniguchi，N.等人（1995）Proc，Natl. Acad，Sci.联合S. A. 92，8754-8758）。在这项研究中，研究了GnT-III基因转移对E-钙粘蛋白的影响，因为E-钙粘蛋白作为转移的抑制因子。高表达GnT-III活性的B16-hm细胞在细胞接触处的E-cadherin表达高于对照组，而不影响转录，凝集素印迹显示来自GnT-III转染子的E-cadherin被异位表达的GnT-III糖基化，与天然E-cadherin相比，糖基化的E-cadherin表现出延迟的更新和减少的从细胞表面的释放，导致GnT-III转染子的细胞-细胞边界处的表达升高。此外，GnT-III转染子中的细胞-细胞聚集增强，表明糖基化的E-cadherin具有生物学功能。这些结果表明，糖基化的E-cadherin有助于通过将GnT-III基因引入黑素瘤细胞来抑制转移。
Introduction of the beta 1-4 N-acetylglucosaminyltransferase (GnT-III) gene was reported to suppress metastasis in highly metastatic B16-hm murine melanoma cells (Yoshimura, M., Nishikawa, A., Ihara, Y., Taniguchi, S., and Taniguchi, N. (1995) Proc, Natl. Acad, Sci. U. S. A. 92, 8754-8758), In this study, the effect of GnT-III gene transfer on E-cadherin was studied, since E-cadherin acts as a suppressor of metastasis. E-cadherin expression at cell-cell contacts of B16-hm cells expressing high GnT-III activity was greater than controls without affecting transcription, Lectin blotting showed that E-cadherin from GnT-III transfectants was glycosylated by ectopically expressed GnT-III, The glycosylated E-cadherin exhibited the delayed turnover and the decreased release from cell surface, as compared with the native E-cadherin, resulting in the elevated expression at the cell-cell border of GnT-III transfectants. Furthermore, cell-cell aggregation was enhanced in GnT-III transfectants, indicating that the glycosylated E-cadherin is biologically functional, These results suggest that the glycosylated E-cadherin contributes to the suppression of metastasis by the introduction of GnT-III gene into melanoma cells.