Choi Sojoong, Kim Yeonhee, Park Haein, Han Inn-Oc, Chung Eunkyung, Lee Sung-Yul, Kim Yong-Bae, Lee Jung Weon, Oh Eok-Soo, Yi Jae Youn
Department of Life Sciences, Division of Life and Pharmaceutical Sciences and the Center for Cell Signaling & Drug Discovery Research, Ewha Womans University, Seoul 120-750, Republic of Korea.
Biochem Biophys Res Commun. 2009 Jun 26;384(2):231-5. doi: 10.1016/j.bbrc.2009.04.093. Epub 2009 Apr 24.
Syndecan-2, a transmembrane heparan sulfate proteoglycan, is known to serve as an adhesion receptor, but details of the regulatory mechanism governing syndecan-2 cell adhesion and migration remain unclear. Here, we examined this regulatory mechanism, showing that overexpression of syndecan-2 enhanced collagen adhesion, cell migration and invasion of normal rat intestinal epithelial cells (RIE1), and increased integrin alpha2 expression levels. Interestingly, RIE1 cells transfected with either syndecan-2 or integrin alpha2 showed similar adhesion and migration patterns, and a function-blocking anti-integrin alpha2 antibody abolished syndecan-2-mediated adhesion and migration. Consistent with these findings, transfection of integrin alpha2 siRNA diminished syndecan-2-induced cell migration in HCT116 human colon cancer cells. Taken together, these results demonstrate a novel cooperation between syndecan-2 and integrin alpha2beta1 in adhesion-mediated cell migration and invasion. This interactive dynamic might be a possible mechanism underlying the tumorigenic activities of colon cancer cells.
Syndecan-2是一种跨膜硫酸乙酰肝素蛋白聚糖，已知其作为一种黏附受体，但调控Syndecan-2细胞黏附和迁移的详细机制仍不清楚。在此，我们研究了这种调控机制，结果显示Syndecan-2的过表达增强了正常大鼠肠上皮细胞（RIE1）的胶原黏附、细胞迁移和侵袭，并提高了整合素α2的表达水平。有趣的是，用Syndecan-2或整合素α2转染的RIE1细胞表现出相似的黏附和迁移模式，并且一种功能阻断性抗整合素α2抗体消除了Syndecan-2介导的黏附和迁移。与这些发现一致，整合素α2小干扰RNA的转染减少了HCT116人结肠癌细胞中Syndecan-2诱导的细胞迁移。综上所述，这些结果证明了Syndecan-2与整合素α2β1在黏附介导的细胞迁移和侵袭中存在新的协同作用。这种相互作用动态可能是结肠癌细胞致瘤活性的潜在机制。
