Molecular mechanism of a cross-talk between estrogen and growth-factor signaling pathways
S Kato, T Kitamoto, Y Masuhiro, J Yanagisawa - Oncology, 1998 - karger.com
S Kato, T Kitamoto, Y Masuhiro, J Yanagisawa
Oncology, 1998•karger.comThe 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 ER and this phosphorylation potentiates the transactivation function
of human ERdemonstrating a novel cross-talk between E2 and growth factor-signaling
pathways. In this review, the molecular mechanism of this cross-talk is discussed.
(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 ER and this phosphorylation potentiates the transactivation function
of human ERdemonstrating a novel cross-talk between E2 and growth factor-signaling
pathways. In this review, the molecular mechanism of this cross-talk is discussed.
Abstract
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 ER and this phosphorylation potentiates the transactivation function of human ERdemonstrating a novel cross-talk between E2 and growth factor-signaling pathways. In this review, the molecular mechanism of this cross-talk is discussed.
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