Kato S, Kitamoto T, Masuhiro Y, Yanagisawa J
Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo, Japan.
Oncology. 1998 Dec;55 Suppl 1:5-10. doi: 10.1159/000055253.
The actions of estrogen (E2) are considered to be mediated through its nuclear E2 receptor (ER). In cancer development, growth factors are shown to act synergistically with E2. Recently, we found that the mitogen-activated protein kinase, activated by growth factors, phosphorylates human ERalpha and this phosphorylation potentiates the transactivation function of human ERalpha demonstrating a novel cross-talk between E2 and growth factor-signaling pathways. In this review, the molecular mechanism of this cross-talk is discussed.
雌激素（E2）的作用被认为是通过其核雌激素受体（ER）介导的。在癌症发展过程中，生长因子被证明与E2协同作用。最近，我们发现由生长因子激活的丝裂原活化蛋白激酶可使人类ERα磷酸化，这种磷酸化增强了人类ERα的反式激活功能，证明了E2与生长因子信号通路之间存在一种新的相互作用。在这篇综述中，将讨论这种相互作用的分子机制。
