Project description:To determine the target genes of KLF5, OE19 cells were treated with either non-targeting siRNA (siNT) or siRNA against KLF5 (siKLF5). RNA was extracted and sequenced.
Project description:ChIP-seq for PPARGC1A was performed in OE19 cells to identify genomic binding sites. Cells were treated with 500 nM lapatinib for 48 hours.
Project description:The genome-wide binding sites of transcription factors provide insight into their regulatory function. We used chromatin immunoprecipitaition with high-throughput sequencing (ChIP-seq) to identify the genomic binding sites of HNF4A and GATA6 in OE19 cells.
Project description:Discovery of genome-wide KLF5 binding sites in the PDCs. Chromatin was obtained from colorectal cancer cell line of one patient, and subjected to ChIP-seq using KLF5, H3K27 antibodies prepared using the NEB Next® ChIP-Seq Library kit (NEB Biolabs) according to the manufacturer’s instructions, and sequenced using the HiSeq 2000 system (Illumina). Raw data from input, KLF5 and H3K27 are uploaded.
Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. ChIP-Seq experiments of KLF5, GATA4 and GATA6 were performed in three gastric cancer cell lines YCC3, AGS and KATOIII
Project description:ChIP-seq for HNF4A, PPARGC1A and H3K27ac was performed in OE19 cells to identify genomic binding sites. Cells were treated with DMSO or 500 nM lapatinib for 48 hours.
Project description:To identify which genes are directly regulated by KLF5 and its acetylation, we performed ChIP-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.
Project description:We used ChIP-seq to map the binding sites of wild-type and mutant KLF5. In addition, by performing H3K27ac ChIP-seq, we mapped the enhancer regions in cell lines of head and neck squamous cell carcinomas, esophageal carcinomas, and stomach adenocarcinomas.
