Project description:NUAK1 was highly expressed in tumors, and promoted their invasion and metastasis.. The study is to explore the downstream of NUAK1 in human gastric cancer SGC-7901 cells
Project description:HPSE plays important roles in gastric cancer cell proliferation, apoptosis and metastasis.The aim of this study is to explore molecular mechanism underling roles of HPSE in gastric cancer cell proliferation, survival, migration and metastasis. SGC-7901 gastric cancer cells were transfected with HPSE siRNA (10nM) or scramble control siRNA, RNA were extracted 24hours after transfectioin and hybridized to Affymetrix microarrays. 3 biological repeats were used for each condition.
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:In order to explore the effect of RNA-binding protein PUM1 on proliferation, metastasis and metabolism of gastric cancer, we established PUM1 stable knockdown SGC-7901 cell lines. We then performed gene expression profiling analysis using data obtained from RNA-seq of PUM1-knockdown and negative control SGC-7901 cells.
Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5 A four chip study using total RNA extracted from SGC-7901 cells transfected with siRNA negative control and SGC-7901 cells knock down of MTA2 with siRNA. Each chip measures the expression level of 45033 genes collected from the authoritative data source including NCBI
Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5
Project description:miR-375 plays an irreplaceable role in regulation of neoplastic progression in gastric cancer. In order to study the mechanism by which miR-375 inhibits the stemness of gastric cancer cell lines, we need to explore the genetic program controlled by miR-375. We used microarrays to detail the global program of gene expression underlying miR-375 up-regulation and identified distinct classes of regulated genes during this process.
Project description:Gastric cancer (GC) is the second leading cause of cancer-related death in the world, but due to the emergence of drug resistance, the chemotherapy effect of GC has not been improved. Hyperthermia (HT) can increase the sensitivity of tumor cells to chemotherapeutic drugs and cause the specific expression of related genes. Therefore, we want to confirm that HT can enhance the sensitivity of SGC-7901/DDP cells to cisplatin (DDP) and explore the molecular mechanism of sensitization. To study the optimal experimental conditions with synergistic effect, temperature gradients (41 ℃, 44 ℃, 47 ℃, 50 ℃), time gradients (12 h, 24 h, 36 h) and DDP concentration gradients (1 μg/ml, 2 μg/ml, 3 μg/ml) were established. Then the microarray analysis was performed to explore the molecular mechanism of HT sensitization. Our results showed that 47 ℃ HT+ 2 μg/ml DDP for 24 h could synergistically inhibit the proliferation of SGC7901/DDP cells and significantly promote early apoptosis. Differentially expressed lncRNAs and mRNAs between groups were obtained. ENST00000434470.1(IDI2-AS1), ENST00000592689.1(TTN-AS1) and ENST00000412526.1(LINC00161) may play a pro-apoptotic role, while asRNAs could be a potential target for the treatment of GC. KEGG pathway enrichment showed that DDP+HT may induce apoptosis of SGC7901/DDP cells through GPCR signaling pathway, BARD signaling pathway and TRAIL signaling pathway. In summary, HT can enhance the sensitivity of SGC-7901/DDP cells to DDP by activating related apoptotic genes and pathways.
Project description:Gastric cancer is one of the most common cancers worldwide, with approximately 1 million patients being diagnosed annually. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of gastric cancer. Since our previous studies indicate that intelectin 1 (ITLN1) is aberrantly expressed in gastric cancer and serves as a prognostic factor for predicting the outcomes of gastric cancer patients, we hypothesized that ITLN1 might participate in the progression and aggressiveness of gastric cancer. We employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer SGC-7901 cells in response to stable over-expression of ITLN1. The results showed that stable over-expression of ITLN1 led to altered expression of 1592 human mRNAs, including 547 up-regulated genes and 1045 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to ITLN1 over-expression in human gastric cancer cells, and these findings will help us understand the pathogenesis of gastric cancer.