Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.
Cancer Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.
Eur J Pharmacol. 2017 Jun 5;804:78-81. doi: 10.1016/j.ejphar.2017.03.026. Epub 2017 Mar 16.
According to the American Society of Clinical Oncology or ASCO's clinical practice guidelines, administration of Tamoxifen for hormone receptor positive patients improved outcomes. However, many studies have been conducted in this issue, with the rise of Tamoxifen resistance in recent decades. There are many alternative growth cascades that are activated in Tamoxifen resistant cells. The most common and well characterized components of such a resistant network are receptor tyrosine kinases, or RTKs, which can influence many other cellular processes. The interactions between estrogen dependent and independent pathways further complicate the networking. MED1, as a member of a mediator complex, which is activated by RTK growth pathways, plays role in co-activating ERα66 to transcribe genes and enhance cellular proliferation. Herein, we will discuss MED1, a novel biomarker which can explain how RTKs interact with ERα66 which results in Tamoxifen resistance.
根据美国临床肿瘤学会（ASCO）的临床实践指南，他莫昔芬（Tamoxifen）可改善激素受体阳性患者的预后。然而，在这个问题上已经进行了许多研究，在过去几十年中，Tamoxifen 耐药性有所上升。在 Tamoxifen 耐药细胞中，有许多替代的生长级联被激活。在这种耐药网络中，最常见和特征最明显的组成部分是受体酪氨酸激酶（RTKs），它可以影响许多其他细胞过程。雌激素依赖性和非依赖性途径之间的相互作用使网络更加复杂。作为由 RTK 生长途径激活的中介复合物的成员，MED1 在共激活 ERα66 转录基因和增强细胞增殖方面发挥作用。在此，我们将讨论 MED1，这是一种新的生物标志物，可以解释 RTKs 如何与 ERα66 相互作用导致 Tamoxifen 耐药。
