Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Cell Adh Migr. 2009 Oct-Dec;3(4):334-6. doi: 10.4161/cam.3.4.9246. Epub 2009 Oct 12.
In addition to mediating cell adhesion, many cell adhesion molecules act as tumor suppressors. These proteins are capable of restricting cell growth mainly through contact inhibition. Alterations of these cell adhesion molecules are a common event in cancer. The resulting loss of cell-cell and/or cell-extracellular matrix adhesion promotes cell growth as well as tumor dissemination. Therefore, it is conventionally accepted that cell adhesion molecules that function as tumor suppressors are also involved in limiting tumor cell migration. Paradoxically, in 2005, we identified an immunoglobulin superfamily cell adhesion molecule hepaCAM that is able to suppress cancer cell growth and yet induce migration. Almost concurrently, CEACAM1 was verified to co-function as a tumor suppressor and invasion promoter. To date, the reason and mechanism responsible for this exceptional phenomenon remain unclear. Nevertheless, the emergence of these intriguing cell adhesion molecules with conflicting roles may open a new chapter to the biological significance of cell adhesion molecules.
除了介导细胞黏附外，许多细胞黏附分子还充当肿瘤抑制因子。这些蛋白质主要通过接触抑制来限制细胞生长。这些细胞黏附分子的改变是癌症的常见事件。由此导致的细胞-细胞和/或细胞-细胞外基质黏附的丧失促进了细胞生长和肿瘤扩散。因此，通常认为作为肿瘤抑制因子的细胞黏附分子也参与限制肿瘤细胞迁移。矛盾的是，在 2005 年，我们鉴定了一种免疫球蛋白超家族细胞黏附分子 hepaCAM，它能够抑制癌细胞生长，同时诱导迁移。几乎同时，CEACAM1 被证实作为肿瘤抑制因子和侵袭促进因子共同发挥作用。迄今为止，导致这种异常现象的原因和机制尚不清楚。然而，这些具有冲突作用的有趣细胞黏附分子的出现可能为细胞黏附分子的生物学意义开辟了一个新篇章。
