Transforming growth factorβ1 transactivates EGFR via an H2O2-dependent mechanism in squamous carcinoma cell line
Transforming growth factorβ1 transactivates EGFR via an H2O2-dependent mechanism in squamous carcinoma cell line
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DOI：
10.1016/j.canlet.2009.08.022
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发表时间：
2010-04-01
期刊：
影响因子：
9.7
通讯作者：
Son, Youngsook
中科院分区：
文献类型：
--
作者：
Lee, EunAh;Yi, Jae Youn;Son, Youngsook
已知TGF β可反激活EGFR。然而，参与这种串扰的信号成分尚未被揭示。在这里，我们发现TGF β(1)在SCC13和A431细胞中以剂量依赖的方式磷酸化EGFR，并且不被egf中和抗体阻断。H2O2被TGF β(1)增加，处理的时间动力学与EGFR激活相同。n -乙酰半胱氨酸预处理可消除TGF β(1)诱导的H2O2诱导和EGFR激活。直接处理H2O2磷酸化EGFR和过氧化氢酶抑制剂可延长TGF β(1)诱导的EGFR激活。这些结果表明，TGF β(1)通过h2o2依赖性机制激活EGFR，进而导致Erk（1/2）的激活。2009爱思唯尔爱尔兰有限公司版权所有。
TGF beta is known to transactivate EGFR. However, the signaling component involved in this crosstalk has yet to be revealed. Here, we found that TGF beta(1) phosphorylated EGFR in a dose-dependent manner in SCC13 and A431 cells, and it was not blocked by EGF-neutralizing antibody. H2O2 was increased by TGF beta(1), treatment in the same time-kinetics as EGFR activation. Pretreatment of N-acetyl cysteine abolished TGF beta(1)-induced H2O2 induction and EGFR activation. Direct treatment of H2O2 phosphorylated EGFR and catalase inhibitor prolonged TGF beta(1)-induced EGFR activation. These results show that TGF beta(1) activates EGFR via an H2O2-dependent mechanism, which subsequently leads to the activation of Erk(1/2). (C) 2009 Elsevier Ireland Ltd. All rights reserved.