Project description:Analysis of ZR-75-1 cells folowing knockdown of EI24 (P53-Induced Gene 8) and control vector. As a p53 response gene, EI24 is known to controlling cell growth, apoptosis, and autophagy. Results provide insight into the role of EI24 in epithelial-to-mesenchymal Parental ZR-75-1 cells, ZR-75-1 cells with shGFP knockdown (control), Two independent clone of knockdown of EI24 in ZR-75-1. All samples are perfomed in duplicate. Total 8 samples exist.
Project description:Testing the hormonal response of ZR-75-1 cells to estrogen, androgens, and a combination of both homones, with view determining the crosstalk between the transcriptional programs mediated by these hormones in breast cancer cells, and comparison with matched ChIP sequencing data for AR and ERalpha. Data analysis demonstrated reciprocal interference between 5α-dihydrotestosterone (DHT)- and estradiol (E2)-induced transcriptional programs. Specifically, regulation of 26% of E2 and 15% of DHT target genes was significantly affected by cotreatment with the other hormone, in the majority of cases (78-83%) antagonistically. Pathway analysis suggested that DHT co-treatment, for example, depleted E2-regulted pathways in cell survival and proliferation. Total RNA was extractd from luminal-like breast cancer ZR-75-1 cells in quadruplicate after treatment for 16h with 10nM of E2, DHT or E2+DHT.
Project description:RNA-sequencing analysis of CDK12 overexpressiong ZR-75-30 cell lines. Cyclin dependent kinase 12 (CDK12) is amplified in approximately 70-90% of HER2 amplified breast cancer. Results provide insight into the targets of CDK12 in HER2 positive breast cancer.
Project description:Testing the hormonal response of ZR-75-1 cells to estrogen, androgens, and a combination of both homones, with view determining the crosstalk between the transcriptional programs mediated by these hormones in breast cancer cells, and comparison with matched ChIP sequencing data for AR and ERalpha. Data analysis demonstrated reciprocal interference between 5α-dihydrotestosterone (DHT)- and estradiol (E2)-induced transcriptional programs. Specifically, regulation of 26% of E2 and 15% of DHT target genes was significantly affected by cotreatment with the other hormone, in the majority of cases (78-83%) antagonistically. Pathway analysis suggested that DHT co-treatment, for example, depleted E2-regulted pathways in cell survival and proliferation.
Project description:Analysis of ZR-75-1 cells folowing knockdown of EI24 (P53-Induced Gene 8) and control vector. As a p53 response gene, EI24 is known to controlling cell growth, apoptosis, and autophagy. Results provide insight into the role of EI24 in epithelial-to-mesenchymal