Project description:The goal of this study is to analyze the expression data from Human gastric cancer cells (BGC‐823) followed by PGRN-downregulation and search potential therapeutic targets of diseases associated with Helicobacter pylori infection
Project description:Metastasis associated 1 family, member 2 (MTA2) gene is classified to metastasis associated gene family. We have previously reported that MTA2 gene was overexpressed in gastric cancer tissues, correlating with tumor invasion, lymph node metastasis, and advanced TNM stage. MTA2 knockdown significantly inhibited gastric cancer cell invasion and metastasis. Yet, its molecular mechanisms are still unclear. The aim of this study is to investigate the molecular mechanisms of MTA2 in regulating malignant behaviors of gastric cancer. This experiment captures the expression data between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells using Whole human genome microarray 4×44K (Design ID: 014850, Agilent technologies).
Project description:Loss of Protocadherin 9 (PCDH9) is associated with the metastasis and the prognosis of gastric cancer patients, while the molecular mechanism of PCDH9-impaired gastric cancer metastasis remains unclear. Here we show that PCDH9 is cleaved in gastric cancer cells and intracellular domain of PCDH9 (PCDH9-Cter) translocates into nucleus. To decipher the mechanism underlying PCDH9-Cter-inhibited tumor cell migration, we performed RNA-Sequencing analysis for BGC-823 cells with or without PCDH9-Cter overexpression.
Project description:Analysis of BGC-823 gastric cancer cells with SIRT1 overexpression or knockdown. SIRT1, a NAD+-dependent protein deacetylase, exerts inhibitory effects on migration and invasion of gastric cancer. Results provide insight into the role of SIRT1 in the metastasis of gastric cancer.
Project description:Cisplatin is the first-line agent utilized for the clinical treatment of a wide variety of solid tumors including gastric cancer. However, the intrinsic or acquired cisplatin resistance is often occurred in patients with gastric cancer and resulted in failure of cisplatin therapy. In order to investigate if miRNA involves in cisplatin resistance of human gastric cancer, we first screened and compared the expression of miRNAs between cisplatin resistant gastric cancer cell lines SGC-7901/DDP and BGC-823/DDP and their sensitive parental cells by miRNAs microarray.
Project description:METTL3-mediated RNA N6-methyladenosine (m6A) is the most prevalent modification participates in tumor initiation and progression via regulating expression of their target genes in cancers.. In this study, we conducted an analysis of m6A microarray in gastric cancer cells.
Project description:The aim of the present study was to identify the candidate genes induced by trichostatin A (TSA) in BGC-823 gastric cancer (GC) cells and to explore the possible inhibition mechanism of TSA in GC. Gene expression data were obtained through chip detection, and differentially expressed genes (DEGs) between GC cells treated with TSA and untreated GC cells (control group) were identified. Gene ontology analysis of the DEGs was performed using the database for annotation, visualization and integrated discovery. Then sub-pathway enrichment analysis was performed and a microRNA (miRNA) regulatory network was constructed. We selected 76 DEGs, among which 43 were downregulated genes and 33 were upregulated genes. By sub-pathway enrichment analysis of the DEGs, the propanoate metabolism pathway was selected as the sub-pathway. By constructing a miRNA regulatory network, we identified that DKK1 and KLF13 were the top hub nodes. The propanoate metabolism pathway and the genes DKK1 and KLF13 may play significant roles in the inhibition of GC induced by TSA. These genes may be potential therapeutic targets for GC. However, further experiments are still required to confirm our results.