Project description:Recent studies suggest that PDEF is required for secretory cell differentiation in several epithelial tissues. To investigate PDEF in the mammary gland, we examined the effect of this transcription factor on gene expression using microarray based profiling of MCF-10A cells. These cells are non-transformed mammary epithelial cells that express protein and gene expression programs of basal epithelial cells and undetectable levels of endogenous PDEF. Bioinformatics analysis of the genes induced or repressed by PDEF overexpression in MCF10A cells revealed a striking effect on expression of luminal and myoepithelial cell markers.
Project description:Recent studies suggest that PDEF is required for secretory cell differentiation in several epithelial tissues. To investigate PDEF in the mammary gland, we examined the effect of this transcription factor on gene expression using microarray based profiling of MCF-10A cells. These cells are non-transformed mammary epithelial cells that express protein and gene expression programs of basal epithelial cells and undetectable levels of endogenous PDEF. Bioinformatics analysis of the genes induced or repressed by PDEF overexpression in MCF10A cells revealed a striking effect on expression of luminal and myoepithelial cell markers. Six samples were harvested 26 hours after retroviral infection with either vector control or PDEF. Each condition was performed in triplicate.
Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF.
Project description:We aimed to identify microRNAs that are regulated by YAP in human mammary epithelial cells. We utilized deep sequencing technology to identify microRNAs that are induced by YAP overexpression and repressed by YAP knockdown.
Project description:Pregnancy-Induced Non-Coding RNA (PINC) is upregulated in alveolar cells of the mammary gland during pregnancy and persist in alveolar cells that remain in the regressed lobules following involution. Here, we show that in the post-pubertal mouse mammary gland, mPINC expression increases throughout pregnancy and then declines in early lactation, when alveolar cells undergo terminal differentiation. Accordingly, mPINC expression is significantly decreased when HC11 mammary epithelial cells are induced to differentiate and produce milk proteins. This natural reduction in mPINC levels may be necessary for lactation, as overexpression of mPINC in HC11 cells blocks lactogenic differentiation, while knockdown of mPINC enhances differentiation. HC11 mammary epithelial cells, with or without knockdown or over-expression of PINC, and with or without treatment by differentiation-inducing agents, were profiled for gene expression.
Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF. Four samples were harvested after lentiviral infection with either non-specific shRNA control or PDEF-targetting shRNA. All samples were subjected to hormone depletion for 48 hours. Each condition was performed in duplicate
Project description:Triple negative breast cancer (TNBC) has poor prognostic outcome compared to other types of breast cancer1. At present the molecular and cellular mechanisms underlying TNBC pathology are not well understood1. Here we report that the transcription factor BCL11A is overexpressed in TNBC including basal-like breast cancer (BLBC) and that its genomic locus is amplified in up to 38% of BLBC tumours. BCL11A overexpression in immortalised human breast epithelial cells promotes tumour formation in xenograft models, whereas knockdown of BCL11A in TNBC cell lines suppresses their tumourigenic potential. In the DMBA-induced mouse mammary tumour model, Bcl11a is found to be essential for tumourigenesis since deletion of Bcl11a before DMBA treatment substantially decreases tumour formation, even in p53-null cells, and inactivation of Bcl11a in established tumours causes their regression. At the cellular level, BCL11A overexpression enhances clonogenicity in vitro whereas its deletion in the mouse causes a reduction in the number of mammary epithelial stem and progenitor cells. Thus, BCL11A has an important role in the genesis of TNBC and in normal mammary epithelial cells. This study highlights the importance of further investigation of BCL11A in breast cancer diagnosis and targeted therapies. [Mouse] KO is bcl11a deleted mammary stem cells. WT are mammary stem cells with intact Bcl11a. [Human] HMLE tumors overexpressing BCL11A.
Project description:The goat of this project is to explore lncRNA55666 efffect on small RNA to regulation goat mammary gland lipid metabolism. We tried to search the mechanism of lncRNA55666 regulation lipid metabolism through miRNA. small RNA seqencing of goat mamamary gland cells samples from different groups: 5NC, lncRNA55666 overexpression, 3NC, lncRNA55666 knockdown. The goat mammary gland cells were cultured in 3D condition. The cell were transfected with virus with lncRNA55666 gene (overexpression), or inhibition of lncRNA expression (lncRNA gene knockdown).