Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out DNA methylation analysis with HumanMethylation450 BeadChip.
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out gene expression analysis with Agilent Human Gene Expression microarray kit.
Project description:Transcriptional profiling of HCT116 cells transfected with either control siRNA or TET1 siRNA was analyzed using whole human genome microarrays. To identify genes regulated by TET1 in colorectal cancer, HCT116 cells were transfected with either control siRNA or TET1 siRNA, and total RNA was extracted from biologically duplicated samples.
Project description:HCT116 is a colorectal cancer cell line. SETDB1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of SETDB1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. SETDB1 is upregulated in cancer cells and promotes cancers. We found that knockdown of SETDB1 in HCT116 cells led to a neuronal-like differentiation phenotype.
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established three stable TET1 knockdown clones and negative control clones of Colo320DM cells, and carried out DNA methylation analysis with HumanMethylation450 BeadChip.
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established three stable TET1 knockdown clones and negative control clones of Colo320DM cells, and carried out gene expression analysis with Agilent Human Gene Expression microarray kit.
Project description:We have demonstrated that ELK4 promted progression and tumorigenesis in colorectal cancer. In order to elucidate the transcriptional regulation mechanism of ELK4 in colorectal cancer, RNA-seq analysis was performed on ELK4 knockdown and control HCT116 cells.
