Mutant epidermal growth factor receptor up-regulates molecular effectors of tumor invasion.
Mutant epidermal growth factor receptor up-regulates molecular effectors of tumor invasion.
复制标题
DOI：
--
复制
发表时间：
2002-06
期刊：
影响因子：
11.2
通讯作者：
A. Lal;Chad A. Glazer;H. Martinson;H. Friedman;G. Archer;J. Sampson;G. Riggins
中科院分区：
文献类型：
--
作者：
A. Lal;Chad A. Glazer;H. Martinson;H. Friedman;G. Archer;J. Sampson;G. Riggins
在人类胶质母细胞瘤中最常改变的基因是表皮生长因子受体（EGFR）。我们分析了由mu EGFR诱导的转录物，以更好地了解其在肿瘤进展中的作用。发现的模式表明增强的肿瘤侵袭。高度诱导的基因包括细胞外基质成分、金属蛋白酶和丝氨酸蛋白酶。我们证实突变的EGFR确实使胶质母细胞瘤细胞更具运动性和侵袭性，使用体外测定。此外，EGFR抑制剂（OSI-774和Tyrphostin AG 1478）选择性下调胶质母细胞瘤细胞中的这些分子效应子，消除了增强的侵袭。
The gene most commonly altered in human glioblastomas is the epidermalgrowth factor receptor (EGFR). We profiled transcripts induced by mutantEGFR to better understand its role in tumor progression. The pattern found suggested enhanced tumor invasion. The highly induced genes included extracellular matrix components, metalloproteases, and a serine protease. We confirmed that mutant EGFR did make glioblastoma cells both more motile and invasive using in vitro assays. Furthermore, inhibitors of EGFR (OSI-774 and Tyrphostin AG1478) selectively down-regulated these molecular effectors in glioblastoma cells, eliminating enhanced invasion.