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Epigenomic characterization of a p53-regulated 3p22.2 tumor suppressor that inhibits STAT3 phosphorylation via protein docking and is frequently methylated in esophageal and other carcinomas
Theranostics ( IF 12.4 ) Pub Date : 2018-01-01 , DOI: 10.7150/thno.20893
Lili Li 1 , Juan Xu 1, 2 , Guohua Qiu 3 , Jianming Ying 1, 4 , Zhenfang Du 1 , Tingxiu Xiang 5 , Kai Yau Wong 6 , Gopesh Srivastava 6 , Xiao-Feng Zhu 7 , Tony S Mok 1 , Anthony Tc Chan 1 , Francis Kl Chan 8 , Richard F Ambinder 3, 9 , Qian Tao 1, 3, 9
Affiliation  

Rationale: Oncogenic STAT3 signaling activation and 3p22-21.3 locus alteration are common in multiple tumors, especially carcinomas of the nasopharynx, esophagus and lung. Whether these two events are linked remains unclear. Our CpG methylome analysis identified a 3p22.2 gene, DLEC1, as a methylated target in esophageal squamous cell (ESCC), nasopharyngeal (NPC) and lung carcinomas. Thus, we further characterized its epigenetic abnormalities and functions.

中文翻译:

p53 调节的 3p22.2 肿瘤抑制因子的表观基因组特征,它通过蛋白质对接抑制 STAT3 磷酸化,并且在食道癌和其他癌症中经常甲基化

基本原理:致癌的 STAT3 信号激活和 3p22-21.3 基因座改变在多种肿瘤中很常见,尤其是鼻咽癌、食道癌和肺癌。这两个事件是否相关尚不清楚。我们的 CpG 甲基化组分析确定了一个 3p22.2 基因DLEC1作为食管鳞状细胞 (ESCC)、鼻咽癌 (NPC) 和肺癌中的甲基化靶标。因此,我们进一步表征了其表观遗传异常和功能。
更新日期:2018-01-01
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