Project description:Ornithogalum is one of the therapeutic formulation used in homeopathic treatments. It is specifically used in the treatment for gastric and duodenal ulcerations. Towards understanding the anticancer mechanism, we investigated the genome-wide mRNA changes upon treating AGS Gastric Cancer cells with Ornithogalum. We observed that totally 707 genes were significantly regulated upon Ornithogalum Treatment, among them 246 genes were upregulated and 461 genes were downregulated. The results provide insight into molecular implication and gene level expression of AGS upon treatment with Ornithogalum. Total RNA was isolated from AGS gastric cancer cells treated with 0.01% of ornithogalum and ethanol control and profiled using Affymetrix Human Gene 1.0 ST Array (HuGene-1_0-st).
Project description:Ornithogalum is one of the therapeutic formulation used in homeopathic treatments. It is specifically used in the treatment for gastric and duodenal ulcerations. Towards understanding the anticancer mechanism, we investigated the genome-wide mRNA changes upon treating AGS Gastric Cancer cells with Ornithogalum. We observed that totally 707 genes were significantly regulated upon Ornithogalum Treatment, among them 246 genes were upregulated and 461 genes were downregulated. The results provide insight into molecular implication and gene level expression of AGS upon treatment with Ornithogalum.
Project description:Gastric cancer is one of the most common cancers worldwide. Epstein-Barr virus-associated gastric cancer accounts for approximately 10% of all gastric cancers. EBV expresses its own proteins and miRNAs (BART miRNAs) and regulates host gene expression. In this study, we examined the effect of EBV infection on host mRNA expression. Differential gene expression was analyzed between EBV-negative human gastric cancer cell line AGS and EBV-positive human gastric cancer cell line AGS-EBV.
Project description:ERK/MAPK pathway is one of the highly activated and a crucial player in gastric cancer proliferation and progression. To delineate the complex transcription program associated with ERK/MAPK pathway, PD98059 a known ERK/MAPK inhibitor was treated in AGS, one of the ERK/MAPK signaling pathway over expressed gastric cancer cell line. The resultant changes in genome-wide mRNA expression pattern between control and PD98059 treated was profiled using Human Gene 1.0 ST arrays.
Project description:Genome-wide mRNA expression profiling was performed in AGS, gastric cancer cell line, upon miR-25 silencing. At 48 hours upon anti-miR-25-3p (miRNA inhibitor) and non-targeting control RNA transfection, the whole transcriptome profiling was performed in triplicates. The miR-25 silencing elevates the diffuse gastric cancer features like expression of COL1A2, expression of COL1A2 co-expressed genes, Epithelial to Mesenchymal Transition (EMT) and angiogenesis associated genes.
Project description:Doxycycline, a tetracycline based antibiotic which has bacteriostatic activity against a broad range of both gram positive and gram negative bacteria was identified to inhibit the expression of ERK/MAPK signaling pathway in gastric cancer. ERK/MAPK pathway is one of the highly activated and a crucial player in gastric cancer progression. To delineate the complex transcription program associated with ERK/MAPK pathway and thus inhibited by doxycycline in gastric cancer cells, doxycycline was treated in AGS, one of the ERK/MAPK overexpressed gastric cancer cell line. The resulatant changes in genome-wide mRNA expression pattern between control and doxycycline treated was profiled using Human Transcriptome 2.0 arrays.
Project description:To determine the role of m6A modification in H.pylori-mediated gastric cancer, we performed RNA methylation immunoprecipitation sequencing (MeRIP-seq) after infecting gastric cancer cell line AGS with H. pylori standard strain Hp26695 at MOI=100 for 12h. The sequencing results include three parts: mRNA, lncRNA, and circRNA.
Project description:AGS gastric cancer cell line was treated with the selective COX-2 inhibitor celecoxib. microRNA expression profile was analyzed between untreated cells and cells treated with celecoxib.
