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Objective To construct the galactose（Gal） and polyethyleneimine（PEI）-modified magnetic nanocarriers（Gal-PEI-SPIO）-mediated c-Met siRNA and to observe its antihepatocarcinoma effect. Methods Gal-PEI-SPIO nanocarriers were prepared and characterized. Agarose gel electrophoresis was used to detect the combination of carriers and siRNA. The cytotoxicity of the nanocarriers was determined by CCK-8. At the same time， q-PCR and Western blotting were used to detect the silencing efficiency of carriers carrying c-Met siRNA in cells. The effects of Gal-PEI-SPIO/c-Met siRNA nanocomposites on the migration and invasion of liver cancer MHCC-97H cells were detected by Transwell chamber method. Result Agarose gel electrophoresis showed that Gal-PEI-SPIO nanocarriers and siRNA could be closely combined when the SPIO： siRNA mass ratio was 4：1 or more. Simultaneously, when the ratio was more than 4：1，the cell activity decreased rapidly. The qPCR results showed that Gal-PEI-SPIO/siRNA nanocomposites effectively reduced the level of mRNA in MHCC-97H cells, and Western blotting showed that the Gal-PEI-SPIO/c-Met siRNA nanocomposites effectively reduced c-Met mRNA and protein levels （all P<0. 01）. In cell invasion and migration experiments, GalPEI-SPIO/c-Met siRNA nanocomposites significantly reduced the invasion and migration abilities of MHCC-97H cells. Conclusion Gal-PEI-SPIO nanocarriers can bind tightly to siRNA, and can carry c-Met siRNA into hepatocellular carcinoma cells to silence c-Met, thereby inhibiting the invasion and migration of MHCC-97H cells. [ABSTRACT FROM AUTHOR]

Objective To screen out th e gastric cancer-related differentially expressed genes ( DEGs), to analyze the biological function and signal pathways, and to explore the relationship between the expression of gastric cancer related core DEGs and the prognosis of gastric cancer. Methods Microarray data of gastric cancer GSE79973 and GSE54129 were downloaded from Gene Expression Omnibus database ( GEO) . We used GE02R to pick out DEGs between gastric cancer and normal gastric tissues. Then we obtained the common DEGs. We used DA YID to analyze the biological functions and signal pathways of DEGs. The protein-protein interaction ( PPI) of these DEGs was constructed by STRING, then we imported it into Cytoscape. The core genes related to gastric cancer were screened out by MCODE plug-in. Finally, we analyzed the overall survival among those core genes. Results There were 164 DEGs in the two datasets, including 42 upregulated genes and 122 down-regulated genes. These DEGs mainly enriched in extracellular region, proteinaceous extracellular matrix, extracellular matrix, and extracellular exosome. They involved in ECM-receptor interaction, focal adhesion, protein digestion and absorption, cytochrome P450 metabolism and other related pathways. Preliminarily, we screened out 13 core genes ( COL1 A2, BGN, THBS2, FNl, THBSl, COLl Al, COIAAl, SPARC, COLl l Al, COL6A3, COL12Al, TIMPl, and SPPl ) related to gastric cancer by MCODE, and 12 of 13 genes had a significantly worse prognosis. Except THBSl, the remaining 12 core genes were significantly associated with poor prognosis of gastric cancer ( all P < 0. 05 ). Conclusions A total of 164 gastric cancer-related DEGs are screened out, including 42 up-regulated genes and 122 down-regulated genes. They are mainly located in extracellular region and proteinaceous extracellular matrix, which are related to ECM-receptor interaction, focal adhesion, and other related pathways, and 12 of 13 gastric cancer-related genes, such as COLI A2, BGN, and THBS2 are associated with poor prognosis of gastric cancer [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of sub-acute exposure to benzene on hematopoietic system in rats and to explore its related mechanism. Methods Thirh male SD rats were raixlomly divided into the blank control group, solvent control group, low-dose benzene group, medium-dose benzene group and high-dose benzene group, with 6 rats in each group. Benzene exposure groups were given 200, 400 and 800 mg/kg benzene solution respectively according to the body mass, the blank control group was not treated, and the solvent control group was given equal volume of corn oil, once a day and for 28 days. Routine blood test was analyzed by automatic blood-counter system. We killed the rats, then calculated the coefficient of liver and spleen, and observed the pathological changes of the femur and the morphological changes of bone marrow and peripheral blood cells. DNA damage of bone marrow and peripheral blood cells were detected by single cell gel electrophoresis (SCGE), and we recorded the tail moment (TM) and Olive tail moment (OTM). Results The WBC of low-dose, medium-dose and high-dose benzene groups were lower than that of the blank control group and the solvent control group (P <0.05). The RBC-in the high-dose benzene group was lower than the other groups, and ihe hemoglobin (Hb) in the medium-dose and high-dose benzene groups was lower than that of the other groups (P < 0.05). There was no significant difference in PLT among these groups (all P > 0.05). There were no significant differences in liver and spleen coefficients among these groups (all P >0.05). In the blank control group and solvent control group, the morphological changes of the bone marrow and peripheral blood cells and the palhologie changes of the bone marrow were basically consistent. The pathological changes showed that in the three benzene groups, the area of hematopoietic tissue was decreased, there were more toxic particles and vacuoles in the bone marrow and peripheral blood cells, meanwhile, with the increased dose of benzene, the above changes were more significant. Compared with the blank control group and solvent control group, TM and OTM were increased in turn in the three benzene groups (P<0. 01). Conclusion Aub-acute ex­posure to benzene has a toxic effect on bone marrow of rats with a dose-dependent manner, which may be rated to DNA damage in peripheral blood and bone marrow cells. [ABSTRACT FROM AUTHOR]

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