Murine mammary gland: PRA transgenics vs. wild-type
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ABSTRACT:
PROVIDER: PRJNA448891 | ENA |
REPOSITORIES: ENA
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Project description:Clinical studies have linked use of progestins (synthetic progesterone (P4)) to breast cancer risk. However, little is understood regarding the role native P4, signaling through the progesterone receptor (PR), plays in formation of breast tumors. Studies published by our lab highlighted a link between PR and immune signaling pathways, suggesting PR induces PR to repress the interferon signaling pathway. Given these findings, we sought to investigate whether P4/PR drive immunomodulation in the mammary gland and development of mammary gland tumors. We found that mice treated with P4 displayed changes in the mammary gland suggesting inhibited immune response compared to placebo-treated mice. Furthermore, transgenic mice with PR overexpression demonstrated decreased numbers of immune cell populations in their mammary gland, lymph nodes, and spleens. Upon long-term monitoring, we determined that multi-parous PR overexpressing mice developed significantly more mammary gland tumors than control mice. Additionally, tumors of PR overexpressing mice contained fewer infiltrating immune cells. Finally, RNA sequencing analysis of tumor samples revealed that immune-related gene signatures were enriched in tumors of control mice compared to tumors of PR overexpressing mice. Together, these findings provide a novel mechanism behind P4-mediated promotion of mammary gland tumor development and provide rationale to investigate anti-progestin treatment to promote immune-mediated elimination of mammary gland tumors.
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2018-12-01 | GSE118467 | GEO
Project description:Mammary gland branching morphogenesis is thought to relie on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive mammary epithelial invasion by remodeling the extracellular matrix and triggering associated signaling cascades. However, the roles that this proteinase plays during postnatal mammary gland development in vivo remain undefined. A mammary gland branching program that occurs during the first 4 weeks of postnatal mouse development, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of deleting epithelial cell Mmp14 on mammary gland morphogenesis. Transcriptome profiling of mammary epithelial cells was used to investigate the functional roles of MT1-MMP in the postnatal mammary epithelial cell compartment in an unbiased fashion
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Project description:The progesterone receptor isoforms PRA and PRB are implicated in breast cancer development and metastasis. Expression ratio PRA/PRB is imbalanced in such cancers under the influence of MAPK-dependent extracellular stimuli that strongly impact progesterone-responsiveM- transcriptional regulation. In order to determine the isoform-specific regulated genes M- in a metastatic cancer cell, we established the iPRAB cell line derived from MDA-MB-231 mammary cancer cells (ER-, PR-). This cell lineM- conditionally expressed PRA and/or PRB under the control of RSL1 and doxycycline (Dox) non-steroid ligands, respectively, in a dose-dependent manner. The bi-inducible expression system was generated using a combination of the Rheoswitch (NE Biolabs) and T-Rex (Invitrogen) vector systems as described in the article. We investigated the transcriptomes obtained in cells treated by either RSL1 (for PRA), or Dox (for PRB), or RSL1 + Dox (for PRA + PRB) for 24 h and then by either 10 nM progesterone (+) or vehicle (-) for 6 h. Control experiments were obtained from cells grown in the absence of RSL1, doxycycline and in the presence of progesterone (O+) or vehicle (O-). Experimental conditions of PRA/PRB expression ratio were ranged from 0.1 to 10, and the maximum expression of a given isoform was set to 300 fmol per mg proteins following 24 h induction. After removing redundant probes and pseudogens, the processed data identified 1014 distinct regulated genes subdivised in 3 classes : genes responding either only to unliganded PR isoforms (-), or only to liganded (+) or to both conditions (mixed M-1). Each classe was subdivided according to isoform specificity criteria (A, B, AB, A&B, A&AB, B&AB, A&B&AB) leading to define 3X7 clusters of genes per classe. Each subset was then further analyzed by complete hierarchical clustering through up or down-regulation criteria. These data indicated that PR target genes selectivity is highly dependent of PRA/PRB expression ratio as well as ligand status and highlight the major impact of PR on transcriptional regulation of genes involved in breast cancer and metastasis.
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Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132 Mammary gland mRNA profiles of Wild Type and Mir-212/132ILN/ILN mice were generated by deep sequencing using Illumina GAIIx.
2014-07-29 | E-GEOD-37952 | biostudies-arrayexpress