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来自复旦大学的研究人员证实,在肝癌中EZH2介导的miR-622丧失决定了CXCR4的激活。这一研究于近日发表在《Nature Communications》杂志上。复旦大学上海医学院徐洁杰博士是这篇论文的通讯作者。miR-622一般是通过靶向K-RAS充当肿瘤抑制子,在人类胃癌组织、胰腺癌及壶腹癌中miR-622下调。CXC趋化因子受体4(CXCR4)和它的趋化因子配体12(CXCL12)在肝癌发展的各个点发挥多种功
Researchers from Fudan University confirmed that EZH2-mediated loss of miR-622 in hepatocellular carcinoma determines CXCR4 activation. The study was recently published in Nature Communications magazine. Dr. Xu Jiejie from Shanghai Medical College of Fudan University is the author of this paper. miR-622 generally targets miR-622 downregulation in human gastric cancer, pancreatic and ampullary cancers by targeting K-RAS as a tumor suppressor. CXC chemokine receptor 4 (CXCR4) and its chemokine ligand 12 (CXCL12) exert a variety of functions at various points in the development of liver cancer