Expression data from MMTV-PyMT Induced Tumors
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE104397 | GEO | 2018/02/22
REPOSITORIES: GEO
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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.
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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.
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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.
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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:The primary cause of mortality in breast cancer is metastasis, a process which is still poorly understood. To study the process of breast cancer metastasis, we isolated focal hyperplasias from the MMTV-PyMT transgenic breast cancer model and transplanted to syngeneic hosts. The transplants underwent stereotyped progression to adenoma, early carcinoma, and late carcinoma at 5, 8 and 18 weeks post-transplant, respectively. We compared the gene expression profiles of adenomas and late carcinomas by microarray. Analysis of the data revealed that the most differentially expressed gene family between adenomas and late carcinomas were luminal differentiation genes, among them GATA-3. Adenomas were uniformly immunopositive for GATA-3, whereas early carcinomas displayed partial loss of GATA-3. Disseminated tumour cells and 18-week late carcinomas were invariably GATA-3 negative. We found that re-introduction of GATA-3 in late carcinomas induced markers of luminal differentiation and inhibited tumour dissemination to distant sites. Keywords: spotted oligonucleotide Full length GATA-3 was cloned into the PMIG retroviral vector, which contains an IRES-GFP cassette. Primary cultures of non-fluorescent MMTV-PyMT carcinomas were infected with the GATA-3 and control retroviruses and transplanted back into the cleared mammary fat pads of wild-type mice. After six weeks of growths, tumors were isolated and total RNA harvested by the Trizol method. Total RNA from GATA-3 infected tumor outgrowths were compared to empty vector infected tumor outgrowths.
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Project description:Expression data from MMTV-PyMT Induced Tumors
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