Project description:Gene expression between DLD1 and DLD1 derived oxaliplatin resistant clones (DLD/OHP1, DLD/OHP4, and DLD/OHP5) was assessed Gene expression between HCT116 and HCT116 derived oxaliplatin resistant clones (HCT/OHP1, HCT/OHP3, and HCT/OHP5) was assessed
Project description:We performed ChIP coupled with high-throughput sequencing (ChIP-seq) for H3K27me3 in DLD1 parental cells and DLD1 p85β K477A/R478A mutant cells
Project description:Whole transciptome analysis of colon cancer mutated cell lines(HCT116 and DLD1) under serum starvation conditions (19hrs-0.5%FBS) We used microarrays to compare gene regulation of truncated cell lines, knocked-out of either the wild type or mutated allele of PI3K, for two independent colon cancer cell lines
Project description:FOXM1 is a key transcription factor regulating cell cycle progression, DNA damage response, and a host of other hallmark cancer features, but the role of the FOXM1 cistrome in driving estrogen receptor-positive (ER+) vs. ER- breast cancer clinical outcomes remains undefined. Chromatin immunoprecipitation sequencing (ChIP-Seq) coupled with RNA sequencing (RNA-Seq) analyses was used to identify FOXM1 target genes in breast cancer cells (MCF-7) where FOXM1 expression was either induced by cell proliferation or repressed by p53 upregulation.
Project description:The Wnt/β-catenin signaling pathway plays crucial roles in nearly all parts of embryonic development and adult stem cell homeostasis. Its aberrant activation has been linked to many diseases such as developmental irregularities and various severe forms of cancer, with colorectal cancer (CRC) as a prime example. While much work has been dedicated to uncovering effective therapeutics to block oncogenic Wnt signaling, such interventions have not proven trivial because of the broad activity of Wnt throughout the adult body and the difficulty in finding suitable molecular targets. We have previously identified the developmental transcription factor TBX3 as a participant of the Wnt-mediated transcriptional regulation. Here we examine the genome-wide binding pattern of TBX3 in the human CRC cells lines HCT116 (25 replicates), DLD1 (2 replicates) and SW620 (2 replicates), by employing CUT&RUN (C&R) with Low-Volume and Urea (LoV-U; Zambanini et al., 2022).
Project description:We report the genome wide DNA binding patterns of wild type FOXM1 in asynchronous HeLa cells using chromatin precipitation followed by high-throughput sequencing (ChIP-seq). We find that FOXM1 is bound to the promoter of a number of cell cycle genes including PLK, AURKB, and CCNB1. FOXM1 ChIP-seq in asynchronous HeLa cells
Project description:The forkhead transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in cancer. Increased levels of FOXM1 are associated with both poor prognosis and oestrogen receptor (ERalpha) status in primary breast cancer. In this study, we map FOXM1 binding genome wide in both ERalpha-positive (MCF-7) and -negative (MDA-MB-231) breast cancer cells. We identify a common set of FOXM1 binding events at cell cycle-regulating genes, but in addition, in MCF-7 cells we find a high level of concordance with ERalpha-binding regions. FOXM1 binding at these co-binding sites is dependent on ERalpha binding, as depletion of ER protein levels reduced FOXM1 binding. FOXM1 interacts directly with both ERalpha co-activator CARM1 and is required for H3 arginine methylation at the ERalpha complex. Inhibition of FOXM1 activity with the ligand thiostrepton resulted in decreased FOXM1 binding at cca. 1400 sites genome wide and reduced expression of genes correlated with poor prognosis in ERalpha-positive tumour samples. These data demonstrate a novel role for the forkhead protein FOXM1 as an ERalpha cofactor and provide insight into the role of FOXM1 in ERalpha-positive breast cancer. The FOXM1-binding sites were mapped by ChIP-Seq in MCF-7 and MDA-MB-231 cells. Cells were treated either with thiostrepton, a FOXM1 inhibitor, or with DMSO (as control). Four replicates were performed in MCF7 cells and two replicates in MDA-MB-231 cells.