Project description:We tried to find the target genes of miR-100 in MGC-803 and SK-BR-3 cells, thus we uesd specific miR-100 inhibitor to knock down the level of miR-100 in the cells, with this condition, we used this mRNA microarray to find the genes whose amount changed. and they may be the target genes that miR-100 mediated. Total of four chips, MGC-AMO, MGC-NC, SK-AMO, SK-NC. MGC and SK represents MGC-803 and SK-BR-3 cells respectively. AMO is the specific miR-100 inhibitor and NC is negative control.
Project description:We tried to find the target genes of miR-100 in MGC-803 and SK-BR-3 cells, thus we uesd specific miR-100 inhibitor to knock down the level of miR-100 in the cells, with this condition, we used this mRNA microarray to find the genes whose amount changed. and they may be the target genes that miR-100 mediated.
Project description:The purpose of this study was to investigate the anti-tumor activity of PEO on MGC-803 cells and its mechanism. Anti-tumor experiments in vitro showed PEO could significantly inhibit the proliferation and migration of MGC-803 cells, and it also could arrest the cell cycle in G2/M phase, decrease the mitochondrial membrane potential and induce apoptosis. Finally, the effects of PEO on genes expression on MGC-803 cells were analyzed by RNA sequencing, and results showed that after treatment with PEO, 100 genes were up-regulated, and 57 genes were down-regulated. According to KEGG pathway and GSEA, FAT4, STK3, LATS2, YAP1 and AJUBA were down-regulated, which are related to HIPPO signaling pathway. Real-time PCR and western blot further confirmed the results of RNA sequencing. These results indicated that PEO may exert anti-tumor activity via the HIPPO/YAP signaling pathway.
Project description:Purpose: Emerging evidence highlights the multifunctional role of noncoding RNAs (ncRNAs) in gastric cancer (GC) chemoresistance. However, the comprehensive expression profile and competing endogenous RNAs (ceRNAs) regulatory network of GC chemoresistance remain unanswered. Methods: The whole-transcriptome sequencing (RNA sequencing) was performed to comprehensively analyze the differentially expressed (DE) lncRNAs, miRNAs and mRNAs in cisplatin-resistant cells MGC-803/DDP and GC cells MGC-803. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted to investigate the biological functions implicated with the DEncRNAs. Then, the cisplatin-resistant-related ceRNA network and potential regulatory axes were constructed by bioinformatic analysis. Results: We successfully generated cisplatin-resistant GC cell line MGC-803/DDP. Differential expression analysis showed that a total of 1,936 DElncRNAs, 2,194 DEmRNAs and 174 DEmiRNAs were identified. Functional enrichment analysis indicated that those DEncRNAs were mainly involved in neuroactive ligand-receptor interaction, drug metabolism and Hippo signaling pathway. Subsequently, the cisplatin-resistant-related ceRNA network was constructed with the widely accepted vital chemo-resistant-related genes and signaling pathways. In addition, two constructed regulatory axes (include FAM66C/miR-129-5p/7 mRNAs and SFTA1P/miR-206/FN1 or NRP1) were successfully validated by the Genomic Data Commons (GDC) GC data. Conclusion: The novel ceRNA network and the potential regulatory axes may provide the most comprehensive view of GC chemoresistance to date. Our findings uncovered potential biomarkers for prognostic prediction and novel therapeutic targets for reversing cisplatin resistance in GC.
Project description:In order to investigate the molecular mechanisms underlying the role of TREM2 in gastric cancer, deep sequencing to profile global gene expression of MGC-803 cells with TREM2 overexpression was performed.
Project description:In order to determine the effect of synbindin on the gene expression profile of gastric cancer cells, MGC-803 cells were infected with adenoviruses carrying either synbindin or GFP. The differentially expressed genes caused by synbindin ectopic expression suggests the underlying mechanism for synbindin-induced cell proliferation.
