Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.
Project description:Colorectal cancer HT-29 cell line is a comonly-used human cancer cell line. We have used this cell line for examining the effect of various anticancer compounds on gene expression and we obtained gene expression data of untreated HT-29 cells as a control data for the analysis.
Project description:Gene(s) in epithelial cells can be upregulated or downregulated by different stimuli in a tissue-specific manner. We used genome-wide microarray analysis to profile the expression of genes in HT-29 cells that are upregulated after stimulation with sodium butyrate (NaB) and subsequently downregulated by the addition of ciprofloxacin antibiotic. The specific aim was to evaluate genes that are associated with mucosal immunity. HT-29 cells were stimulated with sodium butyrate (NaB) (n=3), NaB and ciprofloxacin (n=3) or culture media (unstimulated control, n=3) for 24 hours. RNA extracted from these cells were hybridized on Affymetrix microarrays.
Project description:To elucidate whether F. nucleatum plays a role in colorectal cancer tumorigenesis, RNA-seq analysis was performed to compare the gene expression profiles of F. nucleatum treated HT-29 cell line or not.
Project description:Gene(s) in epithelial cells can be upregulated or downregulated by different stimuli in a tissue-specific manner. We used genome-wide microarray analysis to profile the expression of genes in HT-29 cells that are upregulated after stimulation with sodium butyrate (NaB) and subsequently downregulated by the addition of ciprofloxacin antibiotic. The specific aim was to evaluate genes that are associated with mucosal immunity.
Project description:Aberrant expression of SOX9 in human colorectal cancer cells suggests its roles in the development of colorectal cancer. To gain insight into SOX9-mediated transcriptional regulation in colorectal cancer cells, we attempted to identify its physiological targets on a genome-scale using chromatin immunoprecipitation (ChIP) followed by sequencing (ChIP-seq) in HT-29, human colorectal cancer cells. SOX9 CHIP-seq was carried out using HT-29 cells.
