Expression array of carcinoma cell Mmp14-targeted MMTV-PyMT mammary tumors
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ABSTRACT:
PROVIDER: PRJNA485737 | ENA |
REPOSITORIES: ENA
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Project description:Breast carcinoma cell invasion is thought to depend on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive the remodeling of extracellular matrix and trigger associated signaling cascades. However, the roles that this proteinase plays during breast tumor progression and invasion in vivo remain undefined. A highly penetrant syngeneic mouse model for luminal B breast cancer driven by the polyoma middle T (PyMT) antigen, 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 conditional Mmp14-targeting on breast carcinoma cell invasion programs in vivo. Transcriptome profiling of intact MMTV-PyMT carcinoma tumors was used to investigate the functional roles of carcinoma cell-derived MT1-MMP in MMTV-PyMT tumor progression and invasion in an unbiased fashion
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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:Mammary gland branching morphogenesis is thought to depend on the mobilization of proteolytic machinery from the matrix metalloproteinase (MMP) family, namely MT1-MMP/MMP14, to drive coordinated epithelial cell invasion through the interstitial extracellular matrix, but the dominant effector has remained undefined. Unexpectedly, we find MMP14 controls postnatal mammary gland branching from the periductal stroma. Transcriptome profiling of stromal cell-targeted mammary glands was used to characterize the impact of stromal Mmp14-targeting on the growth factor and signaling cascades implicated in mammary gland morphogenesis. Transcriptome profiling of ductal networks and associated stroma was used to investigate the functional roles of MMP14 in the postnatal mammary gland stroma in an unbiased fashion.
2019-03-01 | GSE79088 | GEO
Project description:Junction Adhesion Molecule-A (JAM-A) is present on leukocytes and platelets where it promotes cell adhesion and motility. We are interested in an interaction between JAM-A and tumor progression/metastases. To address this point, we mated JAM-A-/- mice and mouse mammary tumor model MMTV-PyMT mice which, which express polyoma middle T antigen under the control of mouse mammary tumor virus. MMTV-PyMT mice show 100% penetration of mammary tumor and highly metastases to lung. MMTV-PyMT mice without JAM-A show less primary tumor progression, therefore JAM-A enhance primary tumor progression. Then we are addressing the molecular mechanism of this phenomenon by in vivo. Furthermore, we would like to examine JAM-A deficient MMTV tumor signature. Each 3 MMTV-PyMT JAm-A+/+ (JamA+) and 3 MMTV JAM-A-/- (JamA-) mammary tumor were resected at early stages of tumor development for RNA extraction and hybridization on Affymetrix microarrays.
2010-10-01 | E-GEOD-22555 | biostudies-arrayexpress
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 effects of MMTV-Cre expression on the postnatal mammary epithelial cell compartment in an unbiased fashion
2018-12-01 | GSE118467 | GEO
Project description:Junction Adhesion Molecule-A (JAM-A) is present on leukocytes and platelets where it promotes cell adhesion and motility. We are interested in an interaction between JAM-A and tumor progression/metastases. To address this point, we mated JAM-A-/- mice and mouse mammary tumor model MMTV-PyMT mice which, which express polyoma middle T antigen under the control of mouse mammary tumor virus. MMTV-PyMT mice show 100% penetration of mammary tumor and highly metastases to lung. MMTV-PyMT mice without JAM-A show less primary tumor progression, therefore JAM-A enhance primary tumor progression. Then we are addressing the molecular mechanism of this phenomenon by in vivo. Furthermore, we would like to examine JAM-A deficient MMTV tumor signature.
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Project description:Loss of E2F transcription factos alters metastatic capacity of MMTV-PyMT tumors. We used microarrays to futher characterize the effects of E2F loss on mammary tumorigenesis in MMTV-PyMT mice.
2018-02-22 | GSE104397 | GEO
Project description:The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) loss on the gene expression profiles of tumors from MMTV-Polyomavirus middle-T antigen (PyMT) mice. MMTV-PyMT/S14-heterozygous mice were crossed with S14-heterozygous mice and 1 cm tumors from MMTV-PyMT control (wild-type S14) or MMTV-PyMT/S14-null offspring were profiled using Affymetrix gene arrays. Tumor latency was not different between groups; however, tumors lacking S14 grew significantly slower than control tumors. Loss of S14 also decreased the levels of de novo synthesized fatty acids in mammary tumors. In additional studies, performed on MMTV-Neu mice, we found that S14 overexpression was associated with increased tumor cell proliferation and elevated levels of tumor fatty acids. Gene expression profiling revealed that S14 loss and overexpression in mouse mammary tumors altered pathways associated with proliferation and metabolism. This study provides important information about the role of S14 in mammary tumorigenesis and tumor metabolism. Microarray analysis was performed on 4 mammary tumors from MMTV-PyMT mice and 4 tumors from MMTV-PyMT/S14-null mice.
2014-09-01 | E-GEOD-55886 | biostudies-arrayexpress
Project description:The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) loss on the gene expression profiles of tumors from MMTV-Polyomavirus middle-T antigen (PyMT) mice. MMTV-PyMT/S14-heterozygous mice were crossed with S14-heterozygous mice and 1 cm tumors from MMTV-PyMT control (wild-type S14) or MMTV-PyMT/S14-null offspring were profiled using Affymetrix gene arrays. Tumor latency was not different between groups; however, tumors lacking S14 grew significantly slower than control tumors. Loss of S14 also decreased the levels of de novo synthesized fatty acids in mammary tumors. In additional studies, performed on MMTV-Neu mice, we found that S14 overexpression was associated with increased tumor cell proliferation and elevated levels of tumor fatty acids. Gene expression profiling revealed that S14 loss and overexpression in mouse mammary tumors altered pathways associated with proliferation and metabolism. This study provides important information about the role of S14 in mammary tumorigenesis and tumor metabolism.
2014-09-01 | GSE55886 | GEO
Project description:MicroRNAs (miRNAs) are small noncoding RNAs that typically inhibit the translation and stability of messenger RNAs (mRNAs), controlling genes involved in a variety of cellular processes. miRNA dysregulation is recognized to play an essential role in the development and progression of cancer. MMTV-PyMT mice (Jax Strain: FVB/N-Tg(MMTV-PyVT)634Mul/J) are a well-characterized transgenic mouse model of breast cancer. Upon activation of the MMTV-PyVT transgene (mouse mammary tumor virus (MMTV) long terminal repeat upstream of a cDNA sequence encoding the Polyoma Virus middle T antigen (PyVT)) female carriers develop palpable mammary tumors as early as 5 weeks of age. We performed miRNA microarrays on samples from the MMTV-PyMT transgenic mouse model to investigate the differential expression of miRNAs during development of malignant disease in this model.
2017-08-23 | GSE68630 | GEO