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RNA-seq analysis between mouse UPS tumors (KP) and mouse UPS tumors without HIF-2alpha (KPH2)

ABSTRACT: Purpose: determine RNA expression differences in an unbiased fashion between UPS tumors derived from LSL-KrasG12D;Trp53-/- (KP) mice, and UPS tumors derived from LSL-KrasG12D;Trp53-/-;Epas1-/- (KPH2) mice. Epas1 encodes HIF-2alpha protein.

ORGANISM(S): Mus musculus

PROVIDER: GSE67672 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA280613

REPOSITORIES: GEO

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RNA-seq analysis between mouse UPS tumors (KP) and mouse UPS tumors without HIF-2alpha (KPH2)

Project description:Purpose: determine RNA expression differences in an unbiased fashion between UPS tumors derived from LSL-KrasG12D;Trp53-/- (KP) mice, and UPS tumors derived from LSL-KrasG12D;Trp53-/-;Epas1-/- (KPH2) mice. Epas1 encodes HIF-2alpha protein. RNA-seq was performed on KP (n = 4) and KPH2 (n = 4) derived UPS tumors using Illumina HiSeq 2000.

2015-12-31 | E-GEOD-67672 | biostudies-arrayexpress

HIF-2alpha Knockdown in A498 (VHL-/-) ccRCC cells

Project description:HIF-2alpha is essential for (VHL-/-) ccRCC subcutaneous tumor growth in mice, and in tumor cell lines, its inhibition results in increased ROS accumulation, tumor cell death and responsiveness to radiation treatment. We have utilized transcriptional profiling to screen for putative HIF-2alpha targets genes that serve an anti-oxidant and, thus, cell survival function. A498 ccRCC cell line was treated with control siRNA or mixture of two HIF-2alpha specific siRNA for 48 hours, and RNA was harvested. 4 independent experiments were performed, and expression was compared between control and HIF-2alpha knockdown groups.

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Murine Pancreatic Cancer Cells: KLF10 wild type vs KLF10 knockout

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2016-08-22 | E-GEOD-85521 | biostudies-arrayexpress

Expression data from lung tumors of KrasTgfbr2 -/- mouse model

Project description:Recent data suggests that repression of the Type II TGF-B Receptor (Tgfr2) repression in human lung adenocarcinoma is important for progression from noninvasive to invasive adenocarcinoma. To test this hypothesis in a animal model of non-invasive lung cancer, we generated an inducible, lung specific Tgfbr2 knockout model in the oncogenic Kras mouse. LSL-KrasG12D positive mice were simultaneously backcrossed to C57/Bl6 mice and to the Tgfbr2 flox/flox mice. To induce tumors, 100 _l of saline containing 3x10e10 particles of an adenovirus containing the Cre recombinase (Ad.Cre) was administered to each LSL-KrasG12D mouse intra-nasally.

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Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (miRNA expression)

Project description:We constructed LSL-KrasG12D/+ and Spc-Cre;LSL-KrasG12D/+ mice to investigate the role of microRNA in the pathogenesis of lung cancer

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AP-2alpha-mediated activation of E2F and EZH2 drives melanoma metastasis [ChIP-seq]

Project description:In melanoma metastasis, the role of the AP-2alpha transcription factor, which is encoded by TFAP2A, is controversial as some findings have suggested tumor suppressor activity while other studies have shown high TFAP2A expression in node-positive melanoma associated with poor prognosis. Here we demonstrate that AP-2alpha facilitates melanoma metastasis through transcriptional activation of genes within the E2F pathway including EZH2. A BioID screen found that AP-2alpha interacts with members of the nucleosome remodeling and deacetylase (NuRD) complex. Loss of AP-2alpha removed activating chromatin marks in the promoters of EZH2 and other E2F target genes through activation of the NuRD repression complex. In melanoma cells, treatment witj tazemetostat, an FDA-approved and highly specific EZH2 inhibitor, substantially reduced anchorage-independent colony formation and demonstrated heritable anti-metastatic effects, which were dependent on AP-2alpha. Single cell RNA-seq analysis of a metastatic melanoma mouse model revealed hyperexpansion of Tfap2aHigh/E2F activated cell populations in transformed melanoma relative to progenitor melanocyte stem cells. These findings demonstrate that melanoma metastasis is driven by the AP-2alpha/EZH2 pathway and suggest that AP-2alpha expression can be used as a biomarker to predict responsiveness to EZH2 inhibitors for the treatment of advanced melanomas.

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AP-2alpha-mediated activation of E2F and EZH2 drives melanoma metastasis [RNA-seq]

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2011-09-14 | E-GEOD-27717 | biostudies-arrayexpress

Genome-wide analysis of gene expression in mouse pancreas tumors

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