他莫昔芬在通过GPER/EGFR/ERK/Cyclin D1途径介导的子宫内膜癌具有增生作用：一项回顾性研究和一项体外研究。
摘要来源：
细胞内分泌。 2016 Dec 5 ;437:51-61. Epub 2016 Aug 9. PMID: 27519631
摘要作者：Lizhi Zhang，Yanmin Li，Lan Lan，Rong Liu，Yanhong Wu，Quanxin Qu，Ke Wen
文章隶属关系：lizhi Zhang
摘要:Tamoxifen has been widely used to treat breast cancer as an endocrine therapy. However, tamoxifen is known to enhance the risk of developing endometrial cancer. We want to examine the effect of tamoxifen on endometrial cancer. In our retrospective study, we found that high grade, high stage, and lymph node metastasis were more common in tamoxifen users. In vitro 4-hydroxytamoxifen (OHT) induced cell proliferation and cell cycle promotion in type I and type II endometri所有癌细胞系，并且这种增殖被 GPER 沉默所阻断。 OHT 治疗增加了 EGFR 和 ERK 磷酸化以及细胞周期蛋白 D1 和 GPER 的 mRNA 和蛋白水平。综上所述，我们的数据表明，接受他莫昔芬治疗的子宫内膜癌患者表现出更具侵袭性的组织学亚型和更差的预后。 OHT是子宫内膜癌细胞的增殖诱导剂，GPER/EFGR/ERK/cyclin D1通路参与该过程。