CXCR7/CXCR4 heterodimer-induced histone demethylation: a new mechanism of colorectal tumorigenesis
CXCR7 / CXCR4异源二聚体诱导的组蛋白去甲基化:结直肠肿瘤发生的新机制
作者: Zhi-Yu SongFeng WangShu-Xiang CuiZu-Hua GaoXian-Jun Qu
作者单位: 10000 0004 0369 153X, grid.24696.3f, Department of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China
20000 0004 1936 8649, grid.14709.3b, Department of Pathology, McGill University, Montreal, QC, Canada
30000 0004 0369 153X, grid.24696.3f, Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, China
4grid.414011.1, Department of Pharmacy, Henan Provincial People’s Hospital, Zhengzhou, China
刊名: Oncogene, 2019, Vol.38 (9), pp.1560-1575
来源数据库: Springer Nature Journal
DOI: 10.1038/s41388-018-0519-2
英文摘要: Abstract(#br)Both chemokine receptors (CXCRs) 7 and 4 can facilitate immune cell migration and mediate a vast array of physiological and pathological events. Herein we report, in both human and animal studies, that these two CXCRs can form heterodimers in vivo and promote colorectal tumorigenesis through histone demethylation. Compared with adjacent non-neoplastic tissue, human colorectal cancer (CRC) tissue showed a significant higher expression of CXCR4 and CXCR7, which was colocalized in the cancer cell epithelium. The CXCR/CXCR4 heterodimerization was associated with increased histone demethylase JMJD2A. Villin-CXCR7-CXCR4 transgenic mice demonstrated a greater degree of exacerbated colitis and tumorigenesis than villin-CXCR7 and villin-CXCR4 mice. The CXCR7/CXCR4 heterodimerization...
全文获取路径: Springer Nature  (合作)
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影响因子:7.357 (2012)

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