Project description:We knockout FZR1 in T-47D breast cancer cell line, and treated the knockout and WT cells with cisplatin. The mRNA profiles were analyze.
Project description:Time course of response to synthetic progestin ORG2058 in T-47D and ZR-75-1 breast cancer cell lines and in two PR positive clones of the MCF-10A cell line: AB9 and AB32. Transcriptional response to synthetic progestin, 10nM ORG2058, was compared between the four cell lines at three treatment times. T-47D breast cancer cells were treated in triplicate with 10nM ORG2058 or ethanol vehicle and harvested at 2, 6 and 24h after treatment for gene expression profiling
Project description:We performed RNA-sequencing on 7 tamoxifen-resistant (MCF-7 Tam1, T-47D Tam1, T-47D Tam2, ZR-75-1 Tam1, ZR-75-1 Tam2, BT474 Tam1 and BT-474 Tam2) and their isogenic parental (MCF-7, T-47D, ZR-75-1 and BT-474) breast cancer cell lines. The tamoxifen-resistant cell lines were generated from the parentel cell lines by continuous administration of 1 µM 4-OH-tamoxifen for eight to twelve months. RNA- sequencing was performed to determine the changes in the expression of genes in the resistant clones as well as pathways. In addition, we compared the expression changes of the cell lines with those of the GSE58708 data set which we reanalyzied in our pipeline.
Project description:Bone morphogenetic protein 4 (BMP4) plays an important role in cancer pathogenesis. In breast cancer, it reduces proliferation and increases migration in a cell line-dependent manner. To characterize the transcriptional mediators of these phenotypes, we performed RNA-seq and DNase-seq analyses after BMP4 treatment in MDA-MB-231 and T-47D breast cancer cells that respond to BMP4 with enhanced migration and decreased cell growth, respectively.
Project description:Bone morphogenetic protein 4 (BMP4) plays an important role in cancer pathogenesis. In breast cancer, it reduces proliferation and increases migration in a cell line-dependent manner. To characterize the transcriptional mediators of these phenotypes, we performed RNA-seq and DNase-seq analyses after BMP4 treatment in MDA-MB-231 and T-47D breast cancer cells that respond to BMP4 with enhanced migration and decreased cell growth, respectively.
Project description:We report the chromatin binding sites of HOXB7 transcription factor in BT-474 breast cancer cell line using ChIP-sequencing. We validated the chromatin binding sites in BT-474, MDA-MB-361, MCF7 and T-47D breast cancer cell lines using ChIP-qPCR. The ChIP experiments have been performed using HOXB7 antibody and IgG non-specific antibody as a negative control. The direct downstream target genes of HOXB7 were identified by analyzing the expression of genes located nearby HOXB7 binding sites in HOXB7 knockdown versus control cells using qRT-PCR. Examination of chromatin binding sites of HOXB7 in BT-474 breast cancer cell line using ChIP-seq. Four parallel IgG samples were sequenced, merged together and used as a control data set. Two parallel HOXB7 ChIP samples were sequenced and merged for each replicate, AF1 and AF2. Both HOXB7 ChIP replicates (AF1 and AF2) contained approximately the same amount of reads as the merged IgG control data set.