ObjectiveTo investigate the functional role and underlying molecular mechanisms of fumarylacetoacetate hydrolase （FAH） in the progression of glioblastoma （GBM）. MethodsDifferential expression analysis was performed on the TCGA-GBM， GSE4290， and GSE116520 datasets. Weighted gene co-expression network analysis （WGCNA） was used to identify key modules， and Cox regression and risk modeling were used to screen prognostic genes. Immune infiltration analysis of prognostic genes was carried out by using single-cell RNA sequencing panels. The clinical expression signature of FAH in GBM was analyzed in the TCGA and HPA databases. The functional role of FAH was validated by in vitro and in vivo experiments， and pathway analysis was performed to explore the underlying mechanisms. ResultsA total of 152 overlapping genes were identified across the three GBM datasets （P<0.05）. WGCNA revealed that the turquoise module was most strongly associated with tumor purity， stromal score， immune score， and ESTIMATE score （P<0.001）. Compared with normal tissues， three prognostic genes （CTSD， FAH， and THBD） were upregulated in GBM and correlated with immune infiltration （P<0.05）. FAH mRNA and protein levels were elevated in GBM tissues relative to normal tissues， and its expression was significantly associated with age stratification and TP53 mutation （P<0.05）. CCK-8 assay results showed that， compared with the shNC group， the proliferative activity of GBM cells in the shFAH group was reduced （P<0.001）. Transwell migration and invasion assays demonstrated that， relative to the shNC group， the numbers of migrated and invaded cells in the shFAH group decreased （P<0.05）. Western blot analysis revealed that the protein expression levels of PI3K， p-AKT， and p-mTOR in the shFAH group decreased compared with those in the shNC group （P<0.05）. In vivo subcutaneous xenograft experiments further confirmed that tumor volume and weight significantly decreased in the shFAH group compared with the shNC group （P<0.001）. ConclusionFAH promotes GBM progression by activating the PI3K/AKT/mTOR signaling pathway and may serve as a potential therapeutic target for GBM.

Objective To investigate the gene expressions of IL-1 and TNF-? in bronchoalveolar lavage fluid(BALF) and lung tissues in mice with pulmonary fibrosis(PF) at various periods and to study the effects of cytokines on pulmonary fibrosis.Methods Forty male mice were randomly divided into two groups:experimental group(n=30) and control group(n=10),and poured respectively by bleomycin solutions and saline and killed on the 3rd,7th,14th,28th and 56th day.RT-PCR method was used to analyse the mRNA expressions of IL-1 and TNF-?.Results ① The expressions of IL-1 mRNA and TNF-? mRNA in BALF in experimental group were higher than those in control group(P

Objective Objective To study the effect of Mycobacterium tuberculosis (Mtb) on IFN-? signaling pathway in macrophages. Methods Humans and mice macrophages were isolated and infected by Mtb, condition medium were collected after a few days culture; Macrophage surface expression of Fc?RI (human) or MHC II (mouse) was measured by flow cytometry to explore the effect of condition medium on macrophage response to IFN-?. Results Surface expression of Fc?RI in human macrophages cultured in condition medium was significantly decreased compared to those without condition medium (p

Objective To explore the change of glycogen synthase kinase-3(GSK-3) activity in lymphocytes in patients with mild cognition impairment(MCI).Methods The phosphorylation of GSK-3? at Ser 9 site and total level of GSK-3? in peripheral blood were measured by Western-blot in normal control group,one-year MCI group,two-year MCI group and three-year MCI group.Results The phosphorylation of GSK-3? at Ser 9 site were lower in 1-year MCI group,2-year MCI group and 3-year MCI group,compared with normal control group(all P0.05).Conclusion The activity of GSK-3 in lymphocytes in MCI patients is raised,which implies a subsidiary value of MCI diagnosis.