Project description:ATF1 encodes a sequence-specific activating TF containing a bZIP DNA binding domain, which is overexpressed in CRC tumor tissues compared with their paired normal tissues in two independent cohorts and that ATF1 amplification also frequently occurs across multiple cancer types. Moreover, ATF1 is more highly expressed in advanced stages of CRC. Mechanistically, ATF1 overexpression could provoke cell proliferation and xenograft growth in vitro and in vivo by affecting cell apoptosis, However, the exact mechanism and downstream transcriptional programs by which ATF1 provokes tumor activity are not well understood. We performed ChIP-seq in HCT116cells to investigate the regulatory mechamisms of ATF1.
Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid.
Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid. Two-condition experiment, pchyg vs. 7-2 and 18-2 cells. 1 control, 2 different transfected cells.
Project description:Determination of the ion channel and transporters gene expression profile of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116
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: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:ChIP-seq was performed to profile H4R3me2a occupancy in HCT116 colorectal cancer cells with matched input DNA control. Libraries were sequenced as paired-end 150 bp reads on an Illumina NovaSeq 6000. Reads were aligned to GRCh38 with Bowtie2, peaks were called with MACS2 (q < 0.05), and metagene profiles were generated with deepTools.
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:Here we present the study on ChIP-chip mapping of the genomic binding sites for Sty1, Atf1, and the Atf1's binding partner Pcr1; the genome-wide transcriptional profiling of the atf1 and pcr1 strains in response to H2O2; and the phenotypic assessment of ~90 Atf1/Pcr1-bound or unbound genes for growth fitness under H2O2 conditions. ChIP-chip analysis shows that Atf1 and Pcr1 binding sites are overlapped in the genome and constitutively present before H2O2 stress. On the other hand, Sty1 recruitment primarily occurs at the Atf1/Pcr1 binding sites and is induced by H2O2. We found that Atf1/Pcr1 is clearly responsible for the high-level transcriptional response to H2O2. Furthermore, phenotypic assessment indicates that among the H2O2-induced genes, Atf1/Pcr1-bound genes exhibit a higher likelihood of functional requirement for growth fitness under the stress condition than the Atf1/Pcr1-unbound genes do. Notably, we found that the Atf1/Pcr1-bound genes regardless of their responsiveness to H2O2 show a high probability of requirement for growth fitness. .