Crosstalk Between IGF1R and Estrogen Receptor Signaling in Breast Cancer
Crosstalk Between IGF1R and Estrogen Receptor Signaling in Breast Cancer
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DOI：
10.1007/s10911-008-9098-0
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发表时间：
2008-12-01
影响因子：
2.5
通讯作者：
Yee, Douglas
中科院分区：
文献类型：
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作者：
Fagan, Dedra H.;Yee, Douglas
在发现剥夺某些乳腺肿瘤的雌激素可促进肿瘤消退后，开发了旨在剥夺肿瘤这种激素的治疗策略。雌激素的致瘤性通过雌激素受体α（ER）调节，使理解激活这种受体的机制高度相关。除了雌激素激活ER，其他生长因子途径，如胰岛素样生长因子（IGFs），可以激活ER。本文将探讨这两种途径之间的相互作用。雌激素可以通过ER的基因组和非基因组功能激活IGF途径的生长刺激特性。此外，阻断ER功能可以抑制IGF介导的有丝分裂，阻断IGF作用可以抑制乳腺癌细胞的雌激素刺激。总的来说，这些观察结果表明，这两个生长调节途径是紧密相连的，更彻底地了解这种串扰的机制可能会导致改善乳腺癌的治疗策略。
After the discovery that depriving certain breast tumors of estrogen promoted tumor regression, therapeutic strategies aimed at depriving tumors of this hormone were developed. The tumorigenic properties of estrogen are regulated through the estrogen receptor-alpha (ER), making understanding the mechanisms that activate this receptor highly relevant. In addition to estrogen activating the ER, other growth factor pathways, such as the insulin-like growth factors (IGFs), can activate the ER. This review will examine the interaction between these two pathways. Estrogen can activate the growth stimulatory properties of the IGF pathway via ER's genomic and non-genomic functions. Further, blockade of ER function can inhibit IGF-mediated mitogenesis and blocking IGF action can inhibit estrogen stimulation of breast cancer cells. Collectively, these observations suggest that the two growth regulatory pathways are tightly linked and a more thorough understanding of the mechanism of this crosstalk could lead to improved therapeutic strategies in breast cancer.