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

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

OTHER RELATED OMICS DATASETS IN: GSE101333

PROVIDER: PRJNA394002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5820780.fastq.gz	Fastqsanger.gz
	SRR5820781.fastq.gz	Fastqsanger.gz
	SRR5820782.fastq.gz	Fastqsanger.gz
	SRR5820783.fastq.gz	Fastqsanger.gz
	SRR5820784.fastq.gz	Fastqsanger.gz

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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

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

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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

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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.

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

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RNA-sequencing expression of MMTV-Neu mouse mammary tumors

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Transcriptomic analysis of mammary tumors from MMTV-ErbB2 transgenic mice

Project description:The tyrosine kinase ErbB2 positive breast tumors have more aggressive tumor growth, poorer clinical outcome, and more resistance to radiotherapy, chemotherapy and hormone therapy. A humanized anti-ErbB2 monoclonal antibody Herceptin and a small molecules inhibitor Lapatinib were developed and approved by FDA to treat patients with ErbB2 amplification and overexpression. Unfortunately, most ErbB2+ breast cancers do not respond to Herceptin and Lapatinib, and the majority of responders become resistant within 12 months of initial therapy (defined as secondary drug resistance). Such differences in response to Lapatinib treatment is contributed by substantial heterogeneity within ErbB2+ breast cancers. To address this possibility, we carried out transcriptomic analysis of mammary tumors from genetically diverse MMTV-ErbB2 mice. This will help us to have a better understanding of the heterogeneous response to ErbB2 targeted therapy and permit us to design better and more individualized (personalized) treatment strategies for human ErbB2 positive breast cancer. 214 MMTV-ErbB2 mammary tumors and 8 normal mammary glands were analyzed by Affymetrix microarrays.

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Expression data from MMTV-PyMT Induced Tumors

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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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