Dissecting tumor cell invasion: epithelial cells acquire invasive properties after the loss of uvomorulin-mediated cell-cell adhesion.
Dissecting tumor cell invasion: epithelial cells acquire invasive properties after the loss of uvomorulin-mediated cell-cell adhesion.
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DOI：
10.1083/jcb.108.6.2435
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发表时间：
1989-06
期刊：
影响因子：
--
通讯作者：
Birchmeier W
中科院分区：
文献类型：
--
作者：
Behrens J;Mareel MM;Van Roy FM;Birchmeier W
转化细胞中侵袭力的产生代表了肿瘤进展的重要步骤。在这里，我们表明，首先，非转化的Madin-Darby犬肾（MDCK）上皮细胞获得侵入性的特性时，细胞间粘附被特异性地抑制了细胞粘附分子uvomorulin的抗体，分离的细胞，然后侵入胶原凝胶和胚胎心脏组织。其次，用哈维和莫洛尼肉瘤病毒转化的MDCK细胞是组成型侵袭性的，并且发现它们在其细胞表面不表达uvomorulin。这些数据表明，Uvomorulin（其与E-钙粘蛋白相同，与L-CAM同源）的粘附功能的丧失是促进上皮细胞向更恶性，即，侵入性，表型。在体内癌细胞的侵袭过程中也可能发生类似的细胞间粘附调节。
The generation of invasiveness in transformed cells represents an essential step of tumor progression. We show here, first, that nontransformed Madin-Darby canine kidney (MDCK) epithelial cells acquire invasive properties when intercellular adhesion is specifically inhibited by the addition of antibodies against the cell adhesion molecule uvomorulin; the separated cells then invade collagen gels and embryonal heart tissue. Second, MDCK cells transformed with Harvey and Moloney sarcoma viruses are constitutively invasive, and they were found not to express uvomorulin at their cell surface. These data suggest that the loss of adhesive function of uvomorulin (which is identical to E-cadherin and homologous to L-CAM) is a critical step in the promotion of epithelial cells to a more malignant, i.e., invasive, phenotype. Similar modulation of intercellular adhesion might also occur during invasion of carcinoma cells in vivo.