Project description:This experiment is designed to assess the role of RIP140 in estrogen receptor-dependent gene expression in MCF7 luminal breast cancer cells. MCF7 cells were transfected with an siRNA to target RIP140 or siControl, and subsequently depleted from hormones for three days. Thereafter, cells were treated for 6 hours with 10nM Estradiol and RNA was isolated and further processed for expression analyses.
Project description:To establish a data-driven learning model of the temporal dynamics and 3D chromatin reorganization, we conducted tethered chromatin conformation (TCC) sequencing to examine 3D structure dynamics in estradiol (E2)-induced breast cancer MCF7 cells and Tamoxifen resistant breast cancer MCF7 cells.
Project description:We profiled global PBX1 binding in MCF7 cells. The hypothesis tested was that PBX1 binds regions that recruit ERa following estradiol stimulation. Profiling of PBX1 cistrome in MCF7 breast cancer cells
Project description:We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. However, the relevance of estrogen receptor-beta in mediating endoxifen action has yet to be explored. Therefore, the goals of this study were to determine the differences in the global gene expression profiles elicited by estradiol treatment and endoxifen between parental MCF7 breast cancer cells (expressing estrogen receptor alpha only) and MCF7 cells stably expressing estrogen receptor beta. Total RNA was isolated from parental or estrogen-receptor beta expressing MCF7 cells following 24 hour treatments with either ethanol vehicle, 1nM 17-beta-estradiol or 1nM estradiol plus 40nM endoxifen. All studies were conducted in biological replicates of 2.
Project description:Effect of PBX1 silencing on global gene expression of MCF7 cells stimulated with estradiol. The hypothesis tested was that PBX1 is essential for estrogen signaling in ERa positive breast cancer cells. Total RNA was obtained from MCF7 cells treated with siRNA directed at PBX1 or an siControl for 72h. Cells were then stimulated with estradiol (E2) for 3h prior to RNA extraction.
Project description:Effect of PBX1 silencing on global gene expression of MCF7 cells stimulated with estradiol. The hypothesis tested was that PBX1 is essential for estrogen signaling in ERa positive breast cancer cells.
Project description:Human estrogen-responsive breast cancer cell line MCF-7 wt were used to produce stable clones expressing ER-beta tagged with TAP-tag respectively at the C-term and at the N-term (Ct-ER-beta and Nt-ER-beta) as previously described. MCF7 wt and beta clone cells were cultured in steroid-free medium for 5 days and then were treated with 10nM of 17-beta-estradiol, or vehicle (ETOH). RNA was extracted after 2h, 4h and 8h of stimulation with 17-ß-estradiol 10 nM (+E2) or ethanol vehicle . Total RNA extracted by Ct-ER-beta and Nt-ER-beta cells were pooled (TAP-ER-beta). For mRNA expression profiling, 500 ng total RNA were reverse transcribed and used for synthesis of cDNA and biotinylated cRNA. Finally cRNA were hybridized for 18 hours on Illumina HumanHT-12 v3.0 BeadChips and after scanning, data analysis was performed.
Project description:Quantitative analysis of cellular responses to signaling inhibitors. Total RNA obtained from MCF7 human breast cancer cell lines treated with 1uM gefitinib, 500nM U0126 or 10nM wortmannin for 6hr.