Funato Kosuke, Yamazumi Yusuke, Oda Takeaki, Akiyama Tetsu
Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan.
Exp Ther Med. 2011 May;2(3):457-463. doi: 10.3892/etm.2011.231. Epub 2011 Mar 21.
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 β-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.
PTPRD是一种受体型酪氨酸蛋白磷酸酶。近期对全面突变和拷贝数的分析表明，PTPRD在包括胶质母细胞瘤、黑色素瘤、乳腺癌和结肠癌在内的各种癌症中经常发生突变和纯合缺失。然而，PTPRD在癌症进展中的分子功能尚未阐明。在此，PTPRD抑制结肠癌细胞迁移，并且是适当细胞间粘附所必需的。此外，PTPRD与β-连环蛋白/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，并且与患者生存率显著相关。我们的研究结果表明，PTPRD是结肠癌侵袭和进展所必需的。
