Feedback inhibitors of the epidermal growth factor receptor signaling pathways

Feedback inhibitors of the epidermal growth factor receptor signaling pathways
复制标题

DOI:
10.1016/j.biocel.2008.06.019
复制
发表时间:
2009-03-01
影响因子:
4
通讯作者:
Gotoh, Noriko
Gotoh, Noriko
中科院分区:
生物学2区
文献类型:
--
作者:
Gotoh, Noriko

文献摘要

被引文献

相似文献

表皮生长因子受体家族酪氨酸激酶是细胞增殖和迁移的信号转导通路,参与肿瘤的发生。最近一项广泛的研究强调了复杂的表皮生长因子受体信号网络的负调控因子的主要作用。这些调节器在生理条件下微调信号。当它们的表达受到小丑调控时,由此产生的异常的表皮生长因子受体信号可能会促进细胞的增殖和迁移,从而增加肿瘤的发生。在这篇文章中,我综述了通过多种作用模式优先靶向表皮生长因子受体的特定反馈抑制剂。这些抑制物包括丝裂原诱导基因-6(Mig-6)/受体相关晚期转导(RALT)/基因33、成纤维细胞生长因子受体底物2β(FRS2β)/su1相关神经营养因子靶标-2(SNT-2)/FRS3、细胞因子信号转导抑制因子3(SOCS3)/SOCS4/SOCS5、富亮氨酸重复序列和免疫球蛋白样凝块1(LRIG 1)。尽管关于这些抑制剂的证据还不多,但作为癌症生物标志物,它们可能是有用的,而针对它们的药物的开发肯定会在不久的将来推动个性化药物的发展。(C)2008爱思唯尔有限公司。保留所有权利。
The epidermal growth factor receptor family tyrosine kinases transduce signals for cell proliferation and migration and contribute to tumorigenesis. A recent extensive research has highlighted the major roles of the negative regulators of complex epidermal growth factor receptor signaling networks. These regulators fine-tune signaling under physiological conditions. When their expression is clown regulated, the resultant aberrant epidermal growth factor receptor signaling may promote cell proliferation and migration, leading to increased tumorigenesis. In this paper, I review specific feedback inhibitors that target epidermal growth factor receptors preferentially, via multiple modes of action. The inhibitors include mitogen-inducible gene-6 (Mig-6)/receptor-associated late transducer (RALT)/Gene 33, fibroblast growth factor receptor substrate 2 beta (FRS2 beta)/suc1-associated neurotrophic factor target-2 (SNT-2)/FRS3, sup-pressor of cytokine signaling 3 (SOCS3)/SOCS4/SOCS5, and leucine-rich repeats and immunoglobulin-like clotnains 1 (LRIG 1). Although only fragmentary evidence is available regarding these inhibitors, they might be useful as cancer biomarkers, and the development of drugs that target them would certainly advance personalized medicine in the near future. (C) 2008 Elsevier Ltd. All rights reserved.