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Expression data from mouse breast cancer tissue: Serglycin heterozygous and knock-out conditions

ABSTRACT: Serglycin proteoglycans contribute to proper storage and secretion of inflammatory mediators in hematopoietic cells. Serglycin is also expressed in cancer cells where increased expression has been linked to poor prognosis. In the present study we report that serglycin proteoglycan is absolutely required for metastasis in the MMTV-PyMT-driven mouse breast cancer model. Serglycin seems to play a role in promoting epithelial to mesenchymal transition, cancer-related inflammation and extravasation. Our results suggest that serglycin and serglycin-dependent mediators are potential drug targets to prevent metastatic disease/dissemination of cancer.

ORGANISM(S): Mus musculus

PROVIDER: GSE67806 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA280964

REPOSITORIES: GEO

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Expression data from mouse breast cancer tissue: Serglycin heterozygous and knock-out conditions

Project description:Serglycin proteoglycans contribute to proper storage and secretion of inflammatory mediators in hematopoietic cells. Serglycin is also expressed in cancer cells where increased expression has been linked to poor prognosis. In the present study we report that serglycin proteoglycan is absolutely required for metastasis in the MMTV-PyMT-driven mouse breast cancer model. Serglycin seems to play a role in promoting epithelial to mesenchymal transition, cancer-related inflammation and extravasation. Our results suggest that serglycin and serglycin-dependent mediators are potential drug targets to prevent metastatic disease/dissemination of cancer. 6 total breast tumor samples were analyzed. 3 of SG+/- and 3 of SG-/- tumour tissue. Raw data was normalized using the robust multi-array average (RMA) method. To identify potential serglycin-regulated mediators of metastasis, we performed a microarray expression analysis of RNA isolated from SG+/- and SG-/- breast tumor tissue. The expression analysis identified 672 genes with a significantly altered expression level, at log2 fold >Â±1,2. Strikingly, only six genes were up-regulated in the SG-/- PyMT+ tumor cells compared to SG+/- PyMT+ tumor cells while 666 were significantly down-regulated.

2016-06-01 | E-GEOD-67806 | biostudies-arrayexpress

Characterization of the Chemotherapy-treated PyMT Matrisome

Project description:Cytotoxic chemotherapy is used to treat many thousands of patients across many cancer types annually. Recent studies have demonstrated that chemotherapy causes systemic response that can be exploited to promote cancer cell survival and dissemination, termed “chemotherapy-induced metastasis. However, there have been no studies investigating how chemotherapy alters the extracellular matrix of breast tumors, or if those changes might help to support metastatic dissemination. Here, we report the first characterization of the chemotherapy-treated breast cancer matrisome using the MMTV-PyMT transgenic mouse model of breast cancer. We identify distinct changes induced by different cytotoxic chemotherapies. In particular, we identify collagen IV as significantly associated with taxane-based chemotherapy treatment. Biological validation confirmed collagen IV as chemotherapy-associated and identified collagen IV-driven Src and FAK signaling as important mediators of invasion in the post-chemotherapy tumor microenvironment.

2022-03-14 | PXD032002 | Pride

Single-cell RNA profiling of mammary gland tumours in MMTV-PyMT mouse model of breast cancer.

Project description:Here, we use single cell sequencing to delineate the heterogeneity of tumours from the genetically engineered MMTV-PyMT mouse model of breast cancer (MMTV-PyMT::K14Cre::Rosa-tdTomato mice).

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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 transcriptome analysis of metastatic heterogeneity in a mouse model of breast cancer

Project description:We aimed to understand the transcriptome patterns of organ-derived cancer cell isolates from MMTV-PyMT mice. Tissues from primary tumors and organs harboring distal metastases were harvested from cancer bearing female mice. Although metastatic progression from primary tumors to lung tissue is well studied in the MMTV-PyMT model, metastases to other distal organs and the significance of intratumor heterogeneity across metastases from distal organs remain unclear. To gain insight, we established an array of metastatic cell lines harvested from the MMTV-PyMT breast cancer mouse model. Sequencing at bulk and single-cell level were performed and used to examine the effects of cell heterogeneity on metastases and organ tropism

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Protein difference of breast cancer tissue in mice after radiation therapy and without radiation

Project description:In this study, radiation therapy was performed on mouse breast cancer spontaneous gene mice (MMTV-PyMT) to obtain radiation therapy model of breast cancer mice. To simulate clinical breast cancer radiotherapy and study the differential proteins of breast cancer radiotherapy resistance. MMTV-PyMT mice were randomly divided into two groups, and the radiotherapy group was given the same dose 5 times (3GY, once every 2 days) when the breast cancer tumor grew to an appropriate size (200mm3). The protein extracted from mouse tumor was analyzed by mass spectrometry.

2023-12-06 | PXD047555 |

Multiple anti-tumor programs are activated by blocking BAD phosphorylation: RNA-seq of Bad+/+ or Bad3SA MMTV-PyMT breast tumors

Project description:Purpose: The goals of this study are to compare transcriptome (RNA-seq) differences between wild type and mutant Bad using MMTV-PyMT mouse breast cancer model. Methods: MMTV-PyMT breast cancer model tumors samples (6 independent mice for each genotype) were RNA-sequenced. Reads quality control and alignment to reference genome was done using fastp and STAR aligner respectively. Differentially expressed genes (DEGs) were computed using DESeq2.

2025-04-14 | GSE196626 | GEO

Mechanisms associated with systemic effects of cancer

Project description:Cancer is considered as a disease of a specific organ, but its effects are felt throughout the body. The systemic effects of cancer can lead to weakness in muscles and heart, which hastens cancer-associated death. miR-486 is a myogenic microRNA and its reduced expression in skeletal muscle is observed in muscular dystrophy. Muscle-specific transgenic expression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues skeletal muscle defects in muscular dystrophy animal models. We had previously demonstrated reduced circulating and skeletal muscle levels of miR-486 in several cancer types and lower miR-486 levels correlated with skeletal muscle defects and functional limitations in mammary tumor models. Therefore, skeletal muscle defects induced by cancer could resemble defects observed in various dystrophies, which could be reversed through skeletal muscle expression of miR-486. We performed functional limitations studies and biochemical analysis of skeletal muscles of MMTV-Neu transgenic mice that mimic HER2+ breast cancer and MMTV-PyMT transgenic mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 transgenic mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu, but not in MMTV-PyMT mice. In MMTV-Neu model, miR-486 reversed several of the cancer-induced changes in skeletal muscle including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of phosphorylation of the pre-mRNA processing factor hnRNPA0 and the splicing factor SRSF10. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss-of-function mutation is associated with congenital muscular dystrophy. Thus, similar to muscular dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden in select cancer types.

2022-05-19 | PXD028554 | Pride

Effect of Spot14 Loss on Gene Expression Profile of MMTV-PyMT Mouse Tumors

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

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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.

2010-07-01 | E-GEOD-5223 | biostudies-arrayexpress

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