Project description:This study aimed to identify differential expressed genes before and after treatment with the compound sulforaphene, using the MDA-MB-453 breast cancer cell line as a model.
Project description:This study aimed to identify differential expressed genes before and after treatment with the compound sulforaphene, using the MDA-MB-453 breast cancer cell line as a model. There were a total of 2 samples examined.
Project description:Analysis of MDA-MB-453 breast cancer cells treated with the androgen 5a-dihydrotestosterone (DHT) for 6h, 16h and 48h to define the genes that are differentially regulated in response to DHT.
Project description:Analysis of MDA-MB-453 breast cancer cells treated with the androgen 5a-dihydrotestosterone (DHT) for 6h, 16h and 48h to define the genes that are differentially regulated in response to DHT. MDA-MB-453 breast cancer cells were treated with 5a-dihydrotestosterone (DHT) for time course, followed by RNA extraction and hybridization on Affymetrix microarrays, in order to obtain the gene expression profiles at three time points. The vehicle treated samples are used as control.
Project description:Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. AR and FOXA1 ChIP-seq were performed in MDA-MB-453 breast cancer cells with treatment of 5a-dihydrotestosterone (DHT) for 16 h. TCF7L2 ChIP-seq was performed in MDA-MB-453 cells treated with vehicle or DHT for 16 h, respectively. MYC ChIP-seq was performed in MDA-MB-453 cells following 6 h DHT stimulation.
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ??/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation. AR ChIP was performed in MDA-MB-453 breast cancer cells following 5a-dihydrotestosterone (DHT) stimulation for 4h and 16h respectively. FOXA1 ChIP-seq was performed after 4h DHT stimulation in MDA-MB-453 cells.
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation.
Project description:Triple Negative Breast Cancer (TNBC) is a particular type of breast cancer with the highest mortality rate and there has been growing concern about the development of essential oils as potential anti-cancer drugs.This investigation explored the bioactivity and molecular mechanisms of navel orange peel oil (NOPEO) against TNBC cells. By initiating cell cycle block and apoptosis, NOPEO demonstrated potent growth suppressive properties on the TNBC cell lines MDA-MB-231 and MDA-MB-453. NOPEO was also effective in inhibiting the motility of MDA-MB-231 cells and in down-regulating the levels of MMP-9 and MMP-2 proteins. Additionally, NOPEO's inhibitory effects on MDA-MB-231 gene expression were analysed by RNA sequencing. In total, 1376 genes were found to be upregulated and 1335 genes were downregulated after NOPEO treatment. According to KEGG and GO pathways, the differentially expressed genes were related to MAPK, Jak/stat and FoxQ signalling pathways.
Project description:To investigate single cell transcriptomics of human MDA-MB-453 breast cancer cells in response to the cytokine treatment in compared with the vehicle control
