Project description:To access target binding sites of TEAD4 in gastric cancer, TEAD4 binding was investigated using MKN28 and SNU216 cell lines by ChIP-seq. MKN28 and SNU216 cell lines were cross-linked with formaldehyde, fractionated by sonication and immunoprecipitated by TEAD4 antibody. Immunoprecipitated DNA was prepared by generating libraries and sequenced by massive parallel sequencing.
Project description:To access target binding sites of TEAD4 in gastric cancer, TEAD4 binding was investigated using MKN28 and SNU216 cell lines by ChIP-seq.
Project description:Gene expression profiling of gastric cancer cells MKN28 infected with Sox2 lentivirus comparing with MKN28 infected with control lentivirus Transfected cell lines, MKN28-Sox2 vs. MKN28-NC
Project description:To access oncogenic roles of TEAD4 in gastric cancer, TEAD4-regulated genes were investigated using a SNU216 cell line in which TEAD4 expression was knockdown by shRNA. To compare control to TEAD4 knockdown cell, total RNA was extracted from two cell lines generated by non-silencing shRNA control and TEAD4 knockdown.
Project description:To investigate the function of VPS35 in the regulation of gastric cancer cell proliferation, we established MKN28 cell lines in which VPS35 has been knocked down by shRNA.
Project description:Gene expression profiling of gastric cancer cells MKN28 infected with Sox2 lentivirus comparing with MKN28 infected with control lentivirus
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:To investigate the effect of STAT3 activation on the expression of gastric cancer cells, expression profile was compared in MKN28 cells overexpressed with control vector vs mouse constitutively activated STAT3 mutant (STAT3c). MKN28 gastric cancer cells were transfected with pcDNA3.1 (vector control) or plasmid overexpressing STAT3c (treatment). Stable clones were selected for RNA extraction and expression microarray analysis (Agilent). Experiments were repeated twice.
