Project description:The experiment was to study the gene expression changes in human colorectal cell HCT116 DICER Exon5 knockout cells comparing to that in parental HCT116 cellls. Keywords: Cell type comparison
Project description:The experiment was to study the gene expression changes in human colorectal cell HCT116 DICER Exon5 knockout cells comparing to that in parental HCT116 cellls. Experiment Overall Design: Experiment includes using of two Agilent human 44K microarrays with dye-swap replication.
Project description:A 45h time-course RNA-seq study was performed to analyse the different circadian phenotypes of human colorectal cancer cell line HCT116 WT, HCT116 ARNTL Knockout, HCT116 PER2 Knockout and HCT116 NR1D1 Knockout cells. Samples were taken every 3h starting from 9h after cell synchronization for a period of 45h resulting in 16 time-points for each cell line.
Project description:We employ Mass spectrum to investigate proteome of Pum1-Knockout, Pum2-Knockout and WT conditions in human colorectal cancer cell line Hct116. Overall design: In order to investigate whether Pum1 and Pum2 regulate their targets at their protein levels, we used Pum1-Knockout, Pum2-Knockout and WT Hct116 cell line to extract total protein for Mass spectrum.
Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells Triplicate samples of HCT116 wildtype, HCT116 p53 knockout and HCT116 DICEREX5/EX5 cells were treated with with 0.5 mg/ml of BFA or 2 mg/ml of Tm for 24 h. Following treatment, cells were harvested and lysed in TRIzol reagent and RNA was extracted. Microarray analysis was carried out using Affymetrix HG-U133_Plus-2 arrays.
Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells
Project description:In the present study we have isolated and characterized cancer stem cells and non-cancer stem cells (bulk tumor cells) from high grade human colorectal cancer cell line HCT116 and low grade human colorectal cancer cell line HT29. For this study, cancer stem cells and non-cancer stem cells (bulk tumor cells) were isolated from HCT116 and HT29 human colorectal cancer cell line. For isolating cancer stem cells by FACS, CD44 and CD166 tagged with V450 and PE respectively were used. CD44+CD166+ was the cancer stem cell population and CD44-CD166- was designated as the non-cancer stem cell (bulk tumor cells) population for this study. RNA was isolated from the isolated cell populations and microarray was done to study the whole genome transcriptomic changes.
Project description:We used HCT116 colorectal cancer cells with and without mutations in DNA methyltransferases (resulting in a 95% reduction in global DNA methylation levels) to study the relationship between DNA methylation, histone modifications, and gene expression. (The double knockout cell line is called DKO1) Examination of DNA methylation, two histone modifications, RNA polymerase II ChIP-seq and RNA expression in two cell line (HCT116 and DKO1). One of relipates of HCT116 RNA P II ChIP-seq is from GSM970210. Histone modification data(H3K27ac, H3K4me3) of HCT116 are from GSM945304, GSE31755. Two replicates of RNA-seq data in HCT116 are from GSM1266733 and GSM1266734
