Tyrosine phosphatase PTPRD suppresses colon cancer cell migration in coordination with CD44
Tyrosine phosphatase PTPRD suppresses colon cancer cell migration in coordination with CD44
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DOI：
10.3892/etm.2011.231
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发表时间：
2011-05-01
影响因子：
2.7
通讯作者：
Akiyama, Tetsu
中科院分区：
文献类型：
--
作者：
Funato, Kosuke;Yamazumi, Yusuke;Akiyama, Tetsu
PTPRD是一种受体型酪氨酸蛋白磷酸酶。最近对综合突变和拷贝数的分析表明，PTPRD在各种类型的癌症中经常发生突变和纯合缺失，包括胶质母细胞瘤、黑色素瘤、乳腺癌和结肠癌。然而，PTPRD在癌症进展中的分子功能尚未被阐明。在这里，PTPRD抑制结肠癌细胞的迁移，并且是适当的细胞-细胞粘附所必需的。此外，PTPRD与β -catenin/TCF信号及其靶标CD44协同调节细胞迁移。此外，PTPRD的表达水平在高侵袭性癌症中下调，并与患者生存显著相关。我们的研究结果表明PTPRD是结肠癌侵袭和发展所必需的。
PTPRD is a receptor-type tyrosine-protein phosphatase. Recent analyses of comprehensive mutations and copy numbers have revealed that PTPRD is frequently mutated and homozygously deleted in various types of cancer, including glioblastoma, melanoma, breast and colon cancer. However, the molecular functions of PTPRD in cancer progression have yet to be elucidated. Herein, PTPRD suppressed colon cancer cell migration and was required for appropriate cell-cell adhesion. In addition, PTPRD regulated cell migration in cooperation with beta-catenin/TCF signaling and its target CD44. Furthermore, expression levels of PTPRD were down-regulated in highly invasive cancers and were significantly correlated with patient survival. Our findings suggest that PTPRD is required for colon cancer invasion and progression.