OBJECTIVE: To study the expression of miR-454-3p in colon cancer and its effect on colon cancer proliferation, invasion and hepatic metastasis. METHODS: Specimens of tumor tissues and paired adjacent tissues were collected from 20 patients with colorectal cancer for detecting the expression levels of miR-454-3p using in situ hybridization. Colon cancer cell line SW480 was transfected with a lentiviral vector to induce miR-454-3p over-expression, and the changes in cell proliferation and invasion were observed using cell counting kit-8 (CCK-8), clone formation assay and Transwell experiment. The effect of miR- 454-3p over-expression on hepatic metastasis of colon cancer was assessed in BALB/c mouse models. RESULTS: The results of in situ hybridization showed a significantly increased expression level of miR-454-3p in colon cancer tissues as compared with normal colon tissues ( < 0.05). In SW480 cells, over-expression of miR-454-3p significantly promoted the cell proliferation and invasion ( < 0.05). In BALB/c mice, SW480 cells over-expressing miR-454-3p showed a significantly higher potential for liver metastases than the control cells ( < 0.05). CONCLUSIONS miR-454-3p is overexpressed in the tumor tissues in patients with colorectal cancer and participates in the progression of colorectal cancer by promoting cancer cell proliferation, invasion, and liver metastasis. miR-454-3p may serve as a novel biomarker for colorectal cancer diagnosis and prognostic evaluation.
Animals ; Biomarkers, Tumor ; metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Colon ; metabolism ; Colonic Neoplasms ; metabolism ; pathology ; Disease Progression ; Humans ; Liver Neoplasms ; secondary ; Mice ; Mice, Inbred BALB C ; MicroRNAs ; metabolism ; Neoplasm Invasiveness ; Sincalide ; metabolism

The liver has a strong regenerative capacity,and in case of acute injury,the proliferation of mature hepatocytes helps to complete liver regeneration.However,in case of chronic injury,the proliferative capacity of mature hepatocytes is damaged or exhausted,and the activation,proliferation,and differentiation of hepatic progenitor cells are involved in liver regeneration.This article summarizes the characteristics and origins of hepatic progenitor cells,their role in tissue repair after liver injury and development of liver cancer,and potentials and problems of cell transplantation in the treatment of liver diseases.It is pointed out that an understanding of the biological characteristics of hepatic progenitor cells,their role in liver injury and liver cancer,and related pathogenesis helps with the treatment of liver diseases.

The morbidity and mortality of liver fibrosis induced by a variety of causes remain high around the world and tend to increase year by year. At present, there are no effective radical treatments for liver fibrosis except liver transplantation, and the serious complications of liver fibrosis greatly threaten patients' health and cause a heavy medical burden. Therefore, effective drugs are needed to fight against liver fibrosis. In recent years, great achievements have been made in the research and development of anti-fibrotic drugs and the treatment of liver fibrosis. This article reviews the research advances in drugs and traditional Chinese medicines which act on the different targets of liver fibrosis, inhibit the activation and proliferation of hepatic stellate cells, enhance the activity of matrix metalloproteinase and inhibit the activity of tissue inhibitor of metalloproteinase (TIMP), inhibit inflammatory response, and regulate immune response, as well as the combination of nanoparticles and anti-fibrotic drugs and gene therapy for liver fibrosis.

The disease spectrum of non-alcoholic fatty liver disease (NAFLD) includes non-alcoholic simple fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH),as well as liver cirrhosis and hepatocellular carcinoma,with the most serious type being NASH.The morbidity of NAFLD is seeing an increase year by year in the world,and it is a common cause of chronic hepatic disease and lacks effective treatment.The pathogenesis of NASH is still unknown,and the "two-hit" hypothesis was used to explain the mechanism of NASH.Recent research has found that cholesterol metabolism is closely related to the pathogenesis and severity of NASH.The validity of the "two-hit" hypothesis has been recently challenged,which gives rise to "multi-parallel hit" hypothesis.Cholesterol affects membrane fluidity and membrane protein function through genetic factors,and it can also induce unfolded protein response,and generate toxic oxysterol.Free cholesterol can activate hepatic Kupffer and stellate cells to produce inflammatory cytokines and collagen.The formation of cholesterol crystallization and crown-like structures can damage liver cells and activate Kupffer cells.The above processes can all aggravate liver damage,thus accelerating the development and making the clinical manifestations of NASH even worse.In the present review we summarize the association between cholesterol metabolism and pathogenesis of NASH.