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MMTV tumor and host cells

ABSTRACT: MMTV Wnt-1 and MMTV-Her2 tumors are transplanted onto GFP transgenic mice. Separate GFP+ cells and GFP- cells by FACS sorting to see the oncogene dependent gene expression changes in both tumor cell compartment (GFP- cells). Wnt Fzd 6hrs group: Wnt inhibitor (Fzd8-CRD) treated tumor RNA which will give some clue for direct Wnt target genes only in tumor cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE27540 | GEO | 2012/08/31

SECONDARY ACCESSION(S): PRJNA138559

REPOSITORIES: GEO

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MMTV tumor and host cells

Project description:MMTV Wnt-1 and MMTV-Her2 tumors are transplanted onto GFP transgenic mice. Separate GFP+ cells and GFP- cells by FACS sorting to see the oncogene dependent gene expression changes in both tumor cell compartment (GFP- cells). Wnt Fzd 6hrs group: Wnt inhibitor (Fzd8-CRD) treated tumor RNA which will give some clue for direct Wnt target genes only in tumor cells. GFP- Tumor cells (4 biological replicates) and Wnt-inhibitor treated cells (5 biological replicates)

2012-08-31 | E-GEOD-27540 | biostudies-arrayexpress

Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors

Project description:A transgenic mouse model, MMTV-Wnt/ILK, with mammary specific expression of both Wnt-1 and ILK, was generated by crossing the two mouse lines MMTV-Wnt-1 and MMTV-ILK. Affymetrix Mouse Exon chips were hybridized with material from four independent mammary tumors from each MMTV-Wnt-1 and MMTV-Wnt/ILK transgenic model, in order to identify possible signaling differences involved during increased tumor incidence. One-way ANOVA: MMTV-Wnt vs. MMTV-Wnt/ILK

2010-07-08 | E-GEOD-19300 | biostudies-arrayexpress

Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors

2010-06-16 | GSE19300 | GEO

Changes in Gene expression during the development and progression of mammary tumors in MMTV-Wnt-1 and MMTV-Neu TG mice

Project description:Gene expression profiling of samples from normal virgin mammary glands, hyperplastic mammary glands, mamary tumors, and lung metastases from MMTV-Wnt-1 transgenic (TG) mice, and mammary tumors and lung metastases from MMTV-Neu trangenic (TG) mice Keywords: Array analysis, multi-step tumorigenesis, metastasis, MMTV-Wnt-1 trangenic mice, MMTV-Neu transgenic mice

2005-09-30 | GSE2860 | GEO

Frizzled receptors facilitate Tiki inhibition of Wnt signaling at the cell surface

Project description:Tiki antagonizes Wnt3a signaling by cleaving and inactivating Wnt3a in Wnt-producing cells. Tiki also functions in Wnt-receiving cells to antagonize Wnt signaling by an unknown mechanism. Here, we demonstrate that Tiki inhibition of Wnt signaling at the cell surface requires Frizzled receptors. Tiki associates with the Wnt-FZD complex and cleaves the N-terminus of Wnt3a or Wnt5a, preventing the Wnt-FZD complex from recruiting and activating the coreceptor LRP6 or ROR1/2 without affecting Wnt-FZD complex stability. Intriguingly, we demonstrate that the N-terminus of Wnt3a is required for Wnt3a binding to LRP6 and activating β-catenin signaling, while the N-terminus of Wnt5a is dispensable for recruiting and phosphorylating ROR1/2. Both Tiki enzymatic activity and its association with the Wnt-FZD complex contribute to its inhibitory function on Wnt5a. Our study uncovers the mechanism by which Tiki antagonizes Wnt signaling at the cell surface and reveals a negative role of FZDs in Wnt signaling by acting as Tiki cofactors. Our findings also reveal an unexpected role of the Wnt3a N-terminus in the engagement of the coreceptor LRP6.

2023-05-24 | PXD040942 | Pride

Biomarkers of residual disease, disseminated tumor cells, and metastases in the MMTV-PyMT breast cancer model

Project description:Gene expression profiling of disseminated tumor cells in lung, lung metastatses and residual tumor cells in the MMTV-PyMT breast cancer model. Profiling gene expression change between disseminated tumor cells, lung metastases and residual tumor cells from the MMTV-PyMT breast cancer model.

2013-01-18 | E-GEOD-43566 | biostudies-arrayexpress

Comparative Analysis of MMTV-neu tumors, preneoplastic MMTV-neu mammary gland, and Wild-type controls

Project description:To identify early events of erbB2-induced mammary tumorigenesis, we compared datasets from 14 genechip experiments including MMTV-neu tumors, preneoplastic neu mammary gland (adjacent neu), and age-matched, wild-type control mammary glands Keywords = transgenic mouse Keywords = MMTV-neu Keywords = erbB2 Keywords = HER2 Keywords = mammary tumor Keywords: ordered

2005-05-03 | GSE2528 | GEO

DIMETHYLBENZANTHRACENE (DMBA) INDUCED MAMMARY CARCINOGENESIS IN MMTV-Neu and MMTV/p53 KO FEMALE MICE AND EFFECTS OF REXINOIDS

Project description:Murine models of mammary cancers have proven to be highly informative on numerous fronts including individual gene causation, microenvironmental analyses, and chemoprevention studies. The MMTV-Neu transgenic model of mammary cancer has proven to be a useful model and has been employed in several prevention studies. However, there are certain practical drawbacks to its use including long tumor latencies and a tendency to develop mutations in the transmembrane domain of Neu (unlike human HER2/Neu overexpressing breast cancers). Here we report modifications that were made in an attempt to optimize this mouse model for chemopreventive screening. First, homozygous MMTV-Neu and homozygous P53 KO mice were crossed to create a MMTV-Neu/P53+/- strain (which more closely approximates the genetic make-up of most HER2+ human patients). Second, to overcome the drawback of long tumor latencies, the mice were treated with DMBA for eight weeks. DMBA treatment greatly decreased the latency of mammary carcinomas in the MMTV-Neu mice although the resulting tumors remained histopathologically similar to those from MMTV-Neu control mice. Next, we examined gene expression in tumors derived from MMTV-Neu, MMTV-Neu/p53+/-, and DMBA treated mice. It was found that the characteristic MMTV-Neu tumor-defined expression pattern was still the most prevalent feature of all the MMTV-Neu tumors despite their being crossed to the p53 null allele, treated with DMBA, or both. However, tumors from the DMBA treated animals exhibited many unique gene expression changes including the high expression of stress response, defense, and inflammation genes. Finally, we demonstrated that the RXR agonists UAB30 and Targretin, both inhibited mammary cancer formation in MMTV-Neu mice, including those treated with DMBA. These results demonstrate the potential utility of this murine model for additional chemoprevention studies.

2021-01-31 | GSE35188 | GEO

Expression data of MMTV-PyMT mice mammary tumor with or without JAM-A

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

Small RNA profiling in mouse mammary tumor virus (MMTV) infected cell cultures and induced mammary tumors

Project description:Mouse mammary tumor virus (MMTV) is a complex retrovirus that induces breast cancer in mice in the absence of known virally-encoded oncogenes. Like other non-acute retroviruses, tumorigenesis by MMTV is thought to occur primarily through insertional mutagenesis, leading to the activation of cellular proto-oncogenes and outgrowth of selected cells. In this study, we investigated whether MMTV encodes microRNAs (miRNAs) and/or modulates host miRNAs that could contribute to tumorigenesis. We have applied high throughput small RNA sequencing to the analysis of MMTV-infected cells and MMTV-induced mammary tumors. Our results demonstrate that MMTV does not encode miRNAs. However, MMTV infected cells and MMTV-producing tumors have altered levels of several cellular miRNAs, including increases in the expression of members of the oncogenic miRNA cluster, miR-17-92. Notably, similar changes in levels of these miRNAs have been previously reported in human breast cancers. Combined, our results demonstrate that virally encoded miRNAs do not contribute to MMTV-mediated tumorigenesis, but that changes in specific host miRNAs in infected cells may contribute to virus replication and tumor biology.

2018-02-19 | GSE101333 | GEO

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