本课题组研究发现，金属泛激蛋白1（MPS1）在肝炎、肝硬化、肝癌患者血清中的表达呈上升趋势，其在肝癌患者癌组织中的表达也显著高于癌旁组织；此外，MPS1在肝癌细胞增殖、侵袭、迁移中均发挥作用，而TGF-β刺激肝星形细胞可促进MPS1的表达。基于以往对肝炎、肝癌的研究及国内外相关报道，本课题组推测肝炎中高表达的MPS1可通过激活IL-6/STAT3/GF-β信号通路，诱导TGF-β的表达、分泌，进而促进肝纤维化的发生及肝癌干性；TGF-β又可进一步促进肝星形细胞合成、分泌MPS1，形成正反馈，促进慢性肝炎-肝癌恶性转化。本项目拟扩大样本量，搜集肝炎、肝癌患者血清及随访资料，确认MPS1在慢性肝炎－肝癌恶性转化中作为动态监测指标的可行性；开展细胞实验进行机制研究并通过动物实验加以验证，旨在为慢性肝炎-肝癌恶性转化寻找可靠、无创的动态检测指标，并提供新的治疗靶点，延缓其恶性转化。

Our previous study has found that the expression level of MPS1 (metallopanstimulin-1) in serum of patients with hepatitis, cirrhosis, or hepatic carcinoma shows a upward trend. The expression level of MPS1 in tumor tissue of liver cancer patient is significantly higher than that in paracancer. In addition, MPS1 affect the proliferation, invasion and migration in hepatoma cells. Moreover, transforming growth factor-β (TGF-β) could promote the expression of MPS1 in hepatic stellates cells. Combining previous studies in our group to related reports, we speculate that the expression of MPS1 expressed in hepatitis may promote liver fibrosis and accelerate stemness of hepatic carcinoma by activating IL-6/STAT3/TGF-β signaling pathway, which further promote the expression and secretion of TGF-β. Furthermore, TGF-β could promote the synthesis and secretion of MPS1 in hepatic stellate cells, which forms a positive feedback and further result in malignant transformation from chronic hepatitis to hepatic carcinoma. In this study, we aimed to figure out the role of MPS1 in malignant transformation from chronic hepatitis to hepatic carcinoma by expanding sample size, collecting serum samples, and follow-up information of hepatitis, and the underlying mechanism was explored by experiments both in vitro and in vivo. Founding a reliable and noninvasive detection indicator for malignant transformation from chronic hepatitis to hepatic carcinoma and a new target to intervene or defer the malignant transformation is the target of this study.