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:Specificity protein 1 (SP1) is an essential transcription factor regulating multiple cancer-related genes. Since aberrant expression of SP1 was known to be related to cancer development and progression, we focused on SP1 expression in gastric carcinoma and its correlation with disease outcomes. We discovered a different relationship between SP1 expression and patient survival in intestinal- and diffuse-type gastric cancer. In diffuse-type gastric cancer, patient survival decreased as SP1 expression increased (P < 0.05) in accordance with previously published papers, whereas the lack of SP1 expression in intestinal-type gastric cancer was correlated significantly with poor survival (P < 0.05). When SP1 downregulation was forced in high SP1 expressor intestinal-type gastric cell line MKN28 with siRNA, both migration and invasion were increased but cell proliferation was decreased. In accordance with these results, microarray data in siRNA-transfected MKN28 showed that genes inhibiting migration were downregulated and the expression of genes negatively facilitating proliferation was increased. Both migration and invasion, however, in low SP1 expressor intestinal-type gastric cell line AGS were decreased by forced SP1 expression. In contrast to intestinal-type, in diffuse-type gastric cell line SNU484, high SP1 expressor, both migration and invasion were decreased by siRNA. Contrary to previous studies, which did not reflect differences between the 2 histological types, our results showed that low expression of SP1 is involved in cancer progression and metastasis, and has a different effect on intestinal-type compared to diffuse-type gastric adenocarcinoma. 2 samples for MKN28 cells: si-SP1 against si-control and dyeswap of it upon 72 hour
Project description:Specificity protein 1 (SP1) is an essential transcription factor regulating multiple cancer-related genes. Since aberrant expression of SP1 was known to be related to cancer development and progression, we focused on SP1 expression in gastric carcinoma and its correlation with disease outcomes. We discovered a different relationship between SP1 expression and patient survival in intestinal- and diffuse-type gastric cancer. In diffuse-type gastric cancer, patient survival decreased as SP1 expression increased (P < 0.05) in accordance with previously published papers, whereas the lack of SP1 expression in intestinal-type gastric cancer was correlated significantly with poor survival (P < 0.05). When SP1 downregulation was forced in high SP1 expressor intestinal-type gastric cell line MKN28 with siRNA, both migration and invasion were increased but cell proliferation was decreased. In accordance with these results, microarray data in siRNA-transfected MKN28 showed that genes inhibiting migration were downregulated and the expression of genes negatively facilitating proliferation was increased. Both migration and invasion, however, in low SP1 expressor intestinal-type gastric cell line AGS were decreased by forced SP1 expression. In contrast to intestinal-type, in diffuse-type gastric cell line SNU484, high SP1 expressor, both migration and invasion were decreased by siRNA. Contrary to previous studies, which did not reflect differences between the 2 histological types, our results showed that low expression of SP1 is involved in cancer progression and metastasis, and has a different effect on intestinal-type compared to diffuse-type gastric adenocarcinoma.
Project description:Knock-down or overexpression of LAP2beta regulated migration and invasion of gastric cancer cells in vivo and in vitro studies. To investigate the underlying mechanism for LAP2beta-regulated migration and invasion, we compared the gene expression changes between the mock cells and the stable cells. Total RNA was purified from the mock cells and the stable cells overexpressing LAP2beta
Project description:RNA-binding proteins and their mediated alternative splicing play important roles in tumor cell invasion and migration. Here, we report that ESRP1 is a key regulator of gastric cancer cell metastasis. Overexpression of ESRP1 inhibits the invasion and migration of gastric cancer cells, in vivo and in vitro. Furthermore, we found that ESRP1 causes a wide range of alternative splicing events, and ESRP1-mediated CLSTN1 exon skipping may be a key mechanism for its inhibition of gastric cancer cell invasion and metastasis. Taken together, our data provide a molecular framework for the role of ESRP1 in gastric cancer development.
Project description:Knock-down or overexpression of LAP2beta regulated migration and invasion of gastric cancer cells in vivo and in vitro studies. To investigate the underlying mechanism for LAP2beta-regulated migration and invasion, we compared the gene expression changes between the mock cells and the stable cells.
Project description:RNA-binding proteins and their mediated alternative splicing play important roles in tumor cell invasion and migration. Here, we report that ESRP1 is a key regulator of gastric cancer cell metastasis. Overexpression of ESRP1 inhibits the invasion and migration of gastric cancer cells, in vivo and in vitro. Through crosslinking-immunoprecipitation and high-throughput sequencing (CLIP seq), we revealed that ESRP1 binding to the CLSTN1 mRNA and mediated its exon skipping, which may be a key mechanism for its inhibition of gastric cancer cell invasion and metastasis. Taken together, our data provide a molecular framework for the role of ESRP1 in gastric cancer development.