Molecular mechanisms regulating the hormone sensitivity of breast cancer.
Molecular mechanisms regulating the hormone sensitivity of breast cancer.
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DOI：
10.1111/cas.12521
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发表时间：
2014-11
期刊：
影响因子：
5.7
通讯作者：
Maehara Y
中科院分区：
文献类型：
--
作者：
Tokunaga E;Hisamatsu Y;Tanaka K;Yamashita N;Saeki H;Oki E;Kitao H;Maehara Y
乳腺癌是一种异质性疾病。大约 70% 的乳腺癌呈雌激素受体 (ER) 阳性。内分泌治疗显着改善了 ER 阳性乳腺癌的预后；然而，许多肿瘤表现出对内分泌治疗的从头耐药或获得性耐药。深入了解调节激素敏感性或抵抗的分子机制对于提高内分泌治疗的疗效和克服内分泌治疗的抵抗具有重要意义。生长因子受体信号通路，特别是磷脂酰肌醇 3 激酶 (PI3K)/Akt/哺乳动物雷帕霉素靶点 (mTOR) 通路可以介导对所有形式内分泌治疗的耐药性。相反，FOXA1 转录因子是 ER 功能和内分泌反应的关键决定因素。有趣的是，PI3K/Akt/mTOR 通路诱导的激素抵抗与 FOXA1 功能之间存在联系。本文重点从PI3K/Akt/mTOR通路和FOXA1在乳腺癌激素敏感性调节分子机制方面的功能进行综述。
Breast cancer is a heterogeneous disease. Approximately 70% of breast cancers are estrogen receptor (ER) positive. Endocrine therapy has dramatically improved the prognosis of ER-positive breast cancer; however, many tumors exhibit de novo or acquired resistance to endocrine therapy. A thorough understanding of the molecular mechanisms regulating hormone sensitivity or resistance is important to improve the efficacy of and overcome the resistance to endocrine therapy. The growth factor receptor signaling pathways, particularly the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway can mediate resistance to all forms of endocrine therapy. In contrast, FOXA1 transcription factor is a key determinant of ER function and endocrine response. Intriguingly, a link between hormone resistance induced by the PI3K/Akt/mTOR pathway and the function of FOXA1 has been suggested. In this review, we focus on the PI3K/Akt/mTOR pathway and functions of FOXA1 in terms of the molecular mechanisms regulating the hormone sensitivity of breast cancer.
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