In this study, we proved that the down-regulation of HMGB1 inhibits the invasion of HCCLM6 cells, whereas the up-regulation of HMGB1 enhances the invasion of HCCLM3 cells. In summary, our study evaluated the prognostic significance of HMGB1 expression in numerousspecimens of HCC clinical tissues. As these patients we selected are at early or intermediate stage of HCC patients in our study, the prognostic significance of HMGB1 is related with a part of HCC patients. Immunohistochemical analysis was used to evaluate HMBG1 expression at protein level in these HCC clinical samples. We detected the overexpression of HMGB1 in both HCC cell lines and HCC tissues: the overexpression of HMGB1 was found at both the transcriptional and translational levels. Moreover, the overall survival of our study cohort was significantly poorer in high HMGB1 expression cases than in low HMGB1 expression cases. Therefore, we can infer that HMGB1 expression is a new and independent predictor for HCC patients. Our results indicate that the down-regulation of HMGB1 inhibits the proliferation, migration and invasion of HCCLM6 cells, whereas the upregulation of HMGB1 enhances the proliferation, migration and invasion of HCCLM3 cells. Our finding also provides evidence for molecular target therapy of tumor. In order to completely elucidate the mechanism of carcinogenesis and tumor progression in patients with HCC, further molecular, cellular, and animal model studies should be conducted. Chronic pancreatitis is a progressive inflammatory disorder. The main characteristics of CP are PR-171 acinar injury, leukocyte infiltration and pancreatic fibrosis, in which the destroyed pancreatic secretory parenchyma is replaced by fibrotic tissue, eventually resulting in malnutrition and diabetes. Despite decades of research, no specific therapy is available; the treatment of CP remains empirical. Therefore, better understanding of the mechanisms underlying CP pathophysiology is desired for development of specific and effective therapies. Transforming growth factor -b is a multifunctional protein with a broad spectrum of biological functions in cell growth, differentiation, and extra cellular matrix production. TGF-b plays a promoting role in fibrosis development in the kidney, lung, liver, and pancreas. During CP, TGF-b is secreted by inflammatory cells and injured acinar cells. It activates quiescent pancreatic stellate cells into myofibroblast-like cells. These activated PSCs secrete TGF-b and produce excessive ECM proteins, leading to pancreatic fibrosis. This profibrogenic role of TGF-b is mediated by Smad2/3-dependent and Smad-independent pathway. Therefore, targeting the pathways that can specifically modify or antagonize TGF-b signaling for pancreatic fibrosis development would be a more rational.