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E-GEOD-13274

ABSTRACT: Transcription profiling by array of human mammary epithelial cells infected with a recombinant adenoviral vector expressing a mutated HER2 inactivated for kinase function or wild type HER2

OTHER RELATED OMICS DATASETS IN: PRJNA109591

PROVIDER: E-GEOD-13274 | ExpressionAtlas | 2014-07-03

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-13274-analysis-methods.tsv	Tabular
	E-GEOD-13274-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-13274-configuration.xml	Xml
	E-GEOD-13274-percentile-ranks.tsv	Tabular
	E-GEOD-13274.condensed-sdrf.tsv	Tabular

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Transcription profiling by array of human mammary epithelial cells infected with a recombinant adenoviral vector expressing a mutated HER2 inactivated for kinase function or wild type HER2

Project description:As an oncogene, use of HER2 vaccines in humans requires the development of HER2 immunotherapies with maximal immunologic potential, but minimal oncologic potential. To address these issues, we developed a recombinant adenoviral vector expressing a mutated HER2 inactivated for kinase function (Ad-HER2-ki). Ad-HER2-ki was highly expressed, but non-phosphorylated and elicited minimal transcription dysregulation in primary cells. In contrast, Ad-HER2-wt elicited a strong oncogenic signature associated with tumorigenesis. Experiment Overall Design: Early Passage Human Mammary Epithelial cells (HMECs) were serum starved for 36hrs. and infected at a MOI of 150 with either Ad-GFP, Ad-HER2-wt, or Ad-HER2-ki vectors. At 18 hpi, RNA was extracted and transcriptomes evaluated by microarray. Five samples were infected per virus treatment, each a completely separate biologic replicate.

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Project description:The Epidermal Growth Factor Receptor 2 (ERBB2 or HER2) is amplified and overexpressed in approximately 20% of invasive breast cancers and is associated with metastasis and poor prognosis. Here we describe the role of a constitutively active splice variant of HER2 (Delta-HER2) in human mammary epithelial cells. Overexpression of Delta-HER2 in human mammary cells decreased apoptosis and increased proliferation and expression of epithelial-to-mesenchymal markers. It also induced invasion in three-dimensional cultures and promoted tumorigenicity and metastasis in vivo. In contrast, similar overexpression of wild-type HER2 failed to evoke the same effects. Unbiased protein-tyrosine phosphorylation profiling revealed a significant increase in phosphorylation of several key signaling proteins upon Delta-HER2 expression, some of which not previously shown to belong to the HER2 pathway. In addition, microarray analysis revealed the expression of a set of genes specifically associated with Delta-HER2 expression. We found those genes to be highly expressed in ER-negative, high grade and metastatic primary breast tumors. Altogether, these results provide new insights into the function of a tumorigenic splice variant of HER2 and the signaling cascade deriving from its activity RNA was extracted from MCF10A expressing empty vector, WT-HER2 or Delta-HER2 (n=3).

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Project description:Rho0 HeLa cells (devoid of mitochondrial DNA and functional mitochondria) were infected with recombinant lentiviral vector pLSLG expressing short hairpin RNAi complementary to Exons 3 and 17 of POLRMT gene. 48 hours after infection total RNA was isolated and analyzed for inhibition of POLRMT transcripts by RT-PCR. Total RNA from Rho0 HeLa infected with empty pLSLG vector was used as control. The two samples of RNA were used for microarray hybridization with Affymetrix human genome U133 2.0 plus microarray in order to monitor changes in gene expression patterns after inhibition of POLRMT gene. Keywords: parallel sample

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