Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells
Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells
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DOI：
10.1016/j.bbrc.2006.11.089
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发表时间：
2007-01-26
影响因子：
3.1
通讯作者：
Takai, Yoshimi
中科院分区：
文献类型：
--
作者：
Minami, Yukiko;Ikeda, Wataru;Takai, Yoshimi
正常细胞表现出接触抑制的细胞运动和增殖，但这一点在转化后消失。我们发现，Necl-5最初被确定为脊髓灰质炎病毒受体，在许多癌细胞中上调，它增强了生长因子诱导的细胞运动和增殖。我们发现，当细胞接触其他细胞时，Necl-5以反式方式与Nectin-3相互作用，并通过内吞作用从细胞表面移除，导致细胞运动和增殖减少。我们在这里表明，癌基因V12-Ki-Ras上调编码Necl-5的基因会导致细胞运动和增殖增强。当细胞与细胞接触时，Necl-5的从头合成超过了Necl-5内吞的速度，最终导致细胞表面Necl-5的数量净增加。此外，编码Nectin-3的基因在转化细胞中的表达显著减少。因此，转化后Necl-5的上调有助于转化细胞中接触抑制的丧失。(C)2006 Elsevier Inc.保留所有权利。
Normal cells show contact inhibition of cell movement and proliferation, but this is lost following transformation. We found that Necl-5, originally identified as a poliovirus receptor and up-regulated in many cancer cells, enhances growth factor-induced cell movement and proliferation. We showed that when cells contact other cells, Necl-5 interacts in trans with nectin-3 and is removed by endocytosis from the cell surface, resulting in a reduction of cell movement and proliferation. We show here that up-regulation of the gene encoding Necl-5 by the oncogene V12-Ki-Ras causes enhanced cell movement and proliferation. Upon cell-cell contact, de novo synthesis of Necl-5 exceeds the rate of Necl-5 endocytosis, eventually resulting in a net increase in the amount of Necl-5 at the cell surface. In addition, expression of the gene encoding nectin-3 is markedly reduced in transformed cells. Thus, up-regulation of Necl-5 following transformation contributes to the loss of contact inhibition in transformed cells. (c) 2006 Elsevier Inc. All rights reserved.