Ets-1 expression promotes epithelial cell transformation by inducing migration, invasion and anchorage-independent growth
Ets-1 expression promotes epithelial cell transformation by inducing migration, invasion and anchorage-independent growth
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DOI：
10.1038/sj.onc.1208761
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发表时间：
2005-08-11
期刊：
影响因子：
8
通讯作者：
Wernert, N
中科院分区：
文献类型：
--
作者：
Hahne, JC;Okuducu, AF;Wernert, N
Ets-1是ETS转录因子家族的原型。在人类肿瘤中，Ets-1在肿瘤基质的内皮细胞和成纤维细胞中表达，并被认为通过上调基质降解蛋白酶的表达在肿瘤血管形成和侵袭中发挥作用。在人类肿瘤中，Ets-1也由肿瘤细胞表达，但对这一观察结果的功能意义知之甚少。我们通过稳定选择Ets-1过度表达和低表达的HeLa细胞来解决Ets-1在上皮HeLa肿瘤细胞中的作用。Ets-1的表达增加了HeLa细胞的转化表型，通过促进细胞迁移，侵袭和锚定非依赖性生长，而Ets-1的下调减少了细胞附着。与这些结果相关，Ets-1上调增加整合素β 2的表达，但不增加其他整合素的表达。这些结果表明，除了在肿瘤间质中的作用外，Ets-1还可能通过增加肿瘤转化促进肿瘤的发展和进展。
Ets-1 is the prototype of the family of ETS transcription factors. In human tumors, Ets-1 is expressed in endothelial cells and fibroblasts of the tumor stroma and is proposed to play a role in tumor vascularization and invasion by upregulating expression of matrix-degrading proteases. In human carcinomas, Ets-1 is also expressed by neoplastic cells, but little is known about the functional implications of this observation. We have addressed the role of Ets-1 in epithelial HeLa tumor cells by selecting stably Ets-1 over and underexpressing HeLa cells. Ets-1 expression increases the transformed phenotype of HeLa cells, by promoting cell migration, invasion and anchorage-independent growth, while Ets-1 downregulation reduces cell attachment. In correlation with these results, Ets-1 upregulation increases integrin beta 2 expression but not that of other integrins. These results suggest that, in addition to its role in the tumor stroma, Ets-1 may also promote tumor development and progression by increasing neoplastic transformation.