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OBJECTIVE@#To explore the pathogenesis of gastric cancer through a bioinformatic approach to provide evidence for the prevention and treatment of gastric cancer.@*METHODS@#The differentially expressed genes (DEGs) in gastric cancer and normal gastric mucosa in GSE79973 dataset were analyzed using GEO2R online tool. GO analysis and KEGG pathway enrichment analysis of the DEGs in DAVID database were performed. The protein interaction network was constructed using STRING database, and the key genes (Hub genes) were screened and their functional modules were analyzed using Cytoscape software. The GEPIA database was used to validate the Hub genes, and the Target Scan database was used to predict the microRNAs that regulate the target genes; OncomiR was used to analyze the expressions of the microRNAs in gastric cancer tissues and their relationship with the survival outcomes of the patients.@*RESULTS@#A total of 181 DEGs were identified in gastric cancer, and 10 hub genes were screened by the protein- protein interaction network. Functional analysis showed that these DEGs were involved mainly in protein digestion and absorption, PI3K-Akt signaling pathway, ECM-receptor interaction and platelet activation signal pathway. GEPIA database validation showed that COL1A1 was highly expressed in gastric cancer tissues and was associated with a poor prognosis of patients with gastric cancer. MiR-129-5p was found to bind to the 3'UTR of COL1A1 mRNA, and compared with that in normal tissues, miR-129-5p expression was obviously down-regulated in gastric cancer tissues, and was correlated with the prognosis of the patients.@*CONCLUSIONS@#COL1A1 under regulation by MiR-129-5p is a potential therapeutic target for gastric cancer.
Assuntos
Humanos , Colágeno Tipo I , Biologia Computacional , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , MicroRNAs , Usos Terapêuticos , Fosfatidilinositol 3-Quinases , Neoplasias Gástricas , Tratamento FarmacológicoRESUMO
Objective To detect the M-type phospholipase A2 receptor (PLA2R),and thrombospondin type-1 domain-containing 7A (THSD7A) expression in renal tissue and the levels of their antibodies in adult idiopathic membranous nephropathy (IMN).Also to determine the value of the two markers in the diagnosis of IMN.Methods One hundred and sixteen patients with biopsyproven MN at the Second Hospital of Hebei Medical University from December 2014 to August 2015 were enrolled,including 86 patients with IMN,10 patients with HBV-MN and 10 patients with stage Ⅴ lupus nephritis (LN-Ⅴ).Twenty patients with minimal change disease (MCD) were regarded as control group.We conducted immunohistochemical analysis of the presence of THSD7A and PLA2R the Paraffin section and enzyme linked immunosorbent assay (ELISA) detecting serum PLA2R-AB and THSD7A-AB concentration to investigate whether there was a correlation between them and clinical indicators.Results Compared with the SMN and MCD groups,the positive rates of PLA2R and PLA2R-AB were significantly higher in IMN groups.Expression PLA2R was detected in 88.4％,47.4％,10％ and 0％ and PLA2R-AB in 82.6％,15％,10％,0％,respectively,of the patients with IMN,HBV-MN,LN-Ⅴ and MCD.Expression THSD7A was detected in 2.3％ of the patients with IMN while not detected in SMN and MCD.THSD7A-AB antibody was negative in all patients.Compared with serum PLA2R-Ab negative individuals,patients with serum PLA2R-Ab positive had lower serum albumin (P ＜ 0.001),higher urine protein excretion (P=0.01).The sensitivity of PLA2R-AB,PLA2R,THSD7A and PLA2R+THSD7A in the diagnosis of IMN were 82.6％,88.4％,2.3％,88.6％,and the specificity was 92％,66.7％,100％,66.7％,respectively.Conclusions PLA2R in renal tissue and serum PLA2R-AB are specific markers for the diagnosis of IMN,which are closely related with the severity of IMN.Expression of THSD7A is only positive in some of IMN patients with negative PLA2R,which can be used as a supplementary examination of IMN patients with negative PLA2R.
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Objective:To explore the effect of autophagy inhibitor 3-methyladenine(3-MA) on camptothecin(CPT)-induced Hela cell apoptosis.Methods:MTT assays were carried out to determine the optimal concentration and time of CPT on Hela cells and the effect of different drugs on Hela cell proliferation activity .After Hela cells were treated with different drugs ,the changes of autophagy marker protein( microtubule-associated protein 1 light chain 3,LC3),p62 and apoptosis-related protein were detected using Western blot and immunofluorescence ( IF) .DAPI ( nuclear ) staining was used to observe cell apoptosis rate .Results: In CPC-treated Hela cells,Hela cell proliferation activity declined dramatically ,and autophagy could be induced to occur .Compared with CPT group ,the cell proliferation activity was lower in CPT combined with 3-MA group,the level of autophagy decreased ,but the apoptosis rate significantly increased.Conclusion:CPT can induce autophagy while inducing Hela cell death .Hela cells chemosensitivity to CPT treatment can be enhanced by 3-MA inhibiting autophagy .