Project description:Gastric cancer is one of the most common malignant tumors. Asia has a high incidence of gastric cancer globally. South Korea, Mongolia, Japan and China are the four countries with the highest incidence of gastric cancer in the world. Gansu province in China has the estimated age-standardized incidence rates and mortality rates by Chinese standard population of 62.34/100,000 and 36.94/100,000, respectively, in 2012, which are much higher than the average level of China (22.06/100,000 and 15.16/100,000) in the same year. As a high incidence area of gastric cancer in China, Wuwei city in Gansu province has the prevalence of gastric cancer almost 5 times higher than the average level nationwide. In this study, the cancer tissues and matched adjacent normal mucosa tissues of 5 patients with early gastric cancers who were treated with ESD in Gansu Wuwei Tumor Hospital and the First Hospital of Lanzhou University were collected. All of the patients are from Gansu, China. MicroRNA array was used to find the differences in microRNAs expression profile between the early gastric cancer tissues and the para-cancer normal tissues. It is expected to explore the reasons of the abnormal high incidence of gastric cancer in Gansu Province, China, from the aspect of microRNAs expression profile characteristics.
Project description:Background & Aims: Obesity is the most important risk factor and a potential treatment target for fatty liver disease (FLD). The continuous adaptation or ‘remodelling’ of hepatic mitochondrial flexibility plays a key role in the pathogenesis of FLD. Human adipose stem cell (hASC)-derived hepatocyte-like cells (HLCs) offer attractive tools for the research and therapy of liver dysfunction. However, evidence showing the ‘remodelling’ of hepatic mitochondrial flexibility or differentiation capability of hASCs in obese patients is lacking. Methods: The differentiation capability and mitochondrial structure and function of hepatic cells were evaluated by measuring gene expression, de novo lipogenesis and mitochondrial respiration in HLCs derived from hASCs of obese patients and lean controls. The ability of the GSK3 inhibitor CHIR-99021 to modify the mitochondrial oxidative dysfunction was evaluated in the HLCs derived from the hASCs of obese patients. Results: hASCs from obese patients showed the potential to differentiate into HLCs. HLCs from the hASCs of obese patients exhibited the characteristics of hepatic steatosis, lower expression of the subunits of mitochondrial complex I and lower oxidative phosphorylation levels. CHIR-99021 promoted the expression of NDUFB8, NDUFB9, the subunits of mitochondrial complex I, and the basal oxygen consumption rate of the HLCs derived from the hASCs of obese patients by upregulating the expression of PGC-1α, the transcription factor involved in mitochondrial biogenesis and ‘remodelling’. Conclusions: The results demonstrate that obese patient ASC-derived HLCs had mitochondrial oxidative dysfunction, which may represent the consequence of hepatic steatosis.
