由早期生长反应蛋白1（EGR1）、牙本质基质蛋白1（DMP1）、ARF、p53和PTEN网络介导的肿瘤抑制作用
Tumor suppression by the EGR1, DMP1, ARF, p53, and PTEN Network.
作者信息
Inoue Kazushi, Fry Elizabeth A
机构信息
The Department of Pathology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC, USA.
出版信息
Cancer Invest. 2018;36(9-10):520-536. doi: 10.1080/07357907.2018.1533965. Epub 2018 Nov 5.
Abstract
Recent studies have indicated that EGR1 is a direct regulator of tumor suppressors including TGFβ1, PTEN, and p53. The Myb-like transcription factor Dmp1 is a physiological regulator of the Arf-p53 pathway through transactivation of the promoter and physical interaction of p53. The promoter has binding sites for Egr proteins, and is a target for Dmp1. Crosstalks between p53 and PTEN have been reported. The Egr1-Dmp1-Arf-p53-Pten pathway displays multiple modes of interaction with each other, suggesting the existence of a functional network of tumor suppressors that maintain normal cell growth and prevent the emergence of incipient cancer cells.
摘要
最近的研究表明，EGR1是包括TGFβ1、PTEN和p53在内的肿瘤抑制因子的直接调节因子。Myb样转录因子Dmp1是通过启动子的反式激活和p53的物理相互作用对Arf-p53途径进行生理调节的因子。该启动子具有Egr蛋白的结合位点，并且是Dmp1的作用靶点。已有报道p53和PTEN之间存在相互作用。Egr1-Dmp1-Arf-p53-Pten途径相互之间表现出多种相互作用模式，这表明存在一个维持正常细胞生长并防止初期癌细胞出现的肿瘤抑制因子功能网络。
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