Abnormal differentiation of tumor cells and tyrosine kinase regulation

炎症细胞通过多种炎症介质参与肿瘤的生长和发展。炎性细胞因子激活了核因子-kB和JAK/STAT通路。我们研究了调节细胞因子信号转导的SOCS和Spred家族蛋白在肿瘤发生中的作用。在缺乏SOCS1或SOCS3基因的模型鼠中，我们发现致癌物诱导的肿瘤形成被促进。在人肝细胞癌中，SOCS1和SOCS3基因的表达被沉默。我们还发现，人类SPRED1与I型神经纤维瘤病有关。

Inflammatory cells are involved in tumor growth and development through various inflammatory mediators. Inflammatory cytokines activate the NF-kB and JAK/STAT pathways. We have investigated the function of SOCS family and Spred family proteins which regulate cytokine signaling, on tumorigenesi. In model mice lacking SOCS1 or SOCS3 genes, we found that carcinogen-induced tumorigensis was promoted. In human hepatocellular carcinoma, SOCS1 and SOCS3 gene expression was silenced. We also found that human SPRED1 is responsible for neurofibromatosis type I like disease.