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Mus musculus

ABSTRACT: Oncogenic Hras-dependent epidermal growth is inhibited following RNAi-mediated depletion of Ctnnb1 and Mllt6

PROVIDER: PRJNA210306 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR924492.fastq.gz	Fastqsanger.gz
	SRR924493.fastq.gz	Fastqsanger.gz
	SRR924494.fastq.gz	Fastqsanger.gz
	SRR924495.fastq.gz	Fastqsanger.gz
	SRR924496.fastq.gz	Fastqsanger.gz

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Similar Datasets

Oncogenic Hras-dependent epidermal growth is inhibited following RNAi-mediated depletion of Ctnnb1 and Mllt6

Project description:Genome-wide RNAi screens in mice identified Ctnnb1 and Mllt6 as physiological regulators of HrasG12V-dependent epidermal hyperplasia. To probe the consequences of Ctnnb1 and Mllt6 on HrasG12V-dependent oncogenic growth, we examined how their depletion impacts gene expression in the HrasoncoX2 epidermis. We performed RNA-seq analysis of FACS-purified embryonic epidermal cells, followed by network analysis of differentially regulated transcripts. Whether Ctnnb1 or Mllt6, knockdown markedly enhanced activity of genes restricting growth, and decreased expression of genes promoting epidermal proliferation. This contrasted with known transcriptional changes that typically follow epidermal expression of oncogenic Hras. Moreover, there was a significant overlap in genes whose expression was affected by Mllt6 and β-catenin, further implying a level of shared function. Transcriptional profiles of epidermal progenitors of embryonic day 18.5 animals of wild-type, HrasG12V, and HrasG12V depleted of Ctnnb1 or Mllt6 backgrounds.

2013-07-03 | E-GEOD-48480 | biostudies-arrayexpress

Oncogenic Hras-dependent epidermal growth is inhibited following RNAi-mediated depletion of Ctnnb1 and Mllt6

2013-07-03 | GSE48480 | GEO

Effect of IRE1a and XBP1 knockdown on gene expression in primary mouse keratinocytes expressing an HRas oncogene

Project description:IRE1a is a critical modulator of the unfolded protein response. Its RNAse activity generates the mature transcript for the XBP1 transcription factor and also degrades other ER associated mRNAs in a process termed Regulated IRE1a Dependent mRNA Decay or RIDD. To determine if IRE1a is critical in the response to oncogenic Ras we used ShRNA to knockdown Ire1a or Xbp1 in primary mouse epidermal keratinocytes transduced with a v-HRAS retrovirus.

2017-06-01 | GSE70899 | GEO

CoGAPS matrix factorization algorithm identifies AP-2alpha as a feedback mechanism from therapeutic inhibition of the EGFR network

Project description:Patients with oncogene driven tumors are currently treated with targeted therapeutics such as epidermal growth factor receptor (EGFR) inhibitors. The inhibited oncogenic pathway often interacts with other signaling pathways and alters predicted therapeutic response. Genomic data from The Cancer Genome Atlas (TCGA) demonstrates pervasive molecular alterations to EGFR, MAPK, and PI3K signaling in previously untreated tumors. Therefore, this study uses bioinformatics algorithms to infer the complex pathway interactions that result from EGFR inhibitor use in cancer cells that contain these these common EGFR network genetic alterations. To do this, we modified the HaCaT keratinocyte cell line model of premalignancy to simulate cancer cells with constitutive activation of EGFR, HRAS, and PI3K in a controlled genetic background. We then measured gene expression after treating modified HaCaT cells with three EGFR targeted agents (gefitinib, afatinib, and cetuximab) for 24 hours.

2017-06-12 | GSE80667 | GEO

RNA-seq of heart tissue from 15 day old mice 4 hours post MycER activation compared to wild type controls. RNA-seq of heart tissues from adult mice that have expressed oncogenic H-Ras for 4 weeks followed by MycER activation for 4 hours compared to MycER negative controls.

Project description:Aim: To determine RNA expression levels in the heart of mice 4 hours post Myc activation. Hearts were isolated from 15 day old wild-type (R26+/+) and R26CAG-c-MycERT2/+ mice following 4 hours of MycER activation via administration of (Z)-4-hydroxytamoxifen. Hearts were isolated from adult TetO-HRas; Myh6-tTA; R26CAG-c-MycERT2/+ and TetO-HRas; Myh6-tTA following 4 weeks of oncogenic H-Ras activation (Doxycycline withdrawal) and following 4 hours of MycER activation via administration of (Z)-4-hydroxytamoxifen.

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Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

Homo sapiens

Project description:Oncogenic PI3K mutations lead to NF-kB-dependent cytokine expression following growth

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Transcription profiling of human HCT116 PTEN+/+ cell lines and three independently-derived HCT116 PTEN-/- cell lines

Project description:In an effort to identify genes whose expression is regulated by activated PI3K signaling, we performed microarray analysis and subsequent qRT-PCR on an isogenic set of PTEN gene-targeted human cancer cells. Numerous p53 effectors were upregulated following PTEN deletion, including p21, GDF15, PIG3, NOXA, and PLK2. Stable depletion of p53 led to reversion of the gene expression program. Western blots revealed that p53 was stabilized in HCT116 PTEN-/- cells via an Akt1-dependent and p14ARF-independent mechanism. Stable depletion of PTEN in untransformed human fibroblasts and epithelial cells also led to upregulation of p53 and senescent-like growth arrest. Simultaneous depletion of p53 rescued this phenotype, enabling PTEN-depleted cells to continue proliferating. Next, we tested whether oncogenic PIK3CA, like inactivated PTEN, could activate p53. Retroviral expression of oncogenic human PIK3CA in MCF10A cells led to activation of p53 and upregulation of p53-regulated genes. Stable depletion of p53 reversed these PIK3CA-induced expression changes and synergized with oncogenic PIK3CA in inducing anchorage-independent growth. Finally, targeted deletion of an endogenous allele of oncogenic but not wild-type PIK3CA in a human cancer cell line led to a reduction in p53 levels and a decrease in the expression of p53-regulated genes. These studies demonstrate that activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression in human cells, indicating that p53 can function as a brake on PIP3-induced mitogenesis during human cancer pathogenesis. Experiment Overall Design: Two HCT116 PTEN+/+ cell lines (parental cells and a clone with random integration of the targeting vector) and three independently-derived HCT116 PTEN-/- cell lines were studied

2008-06-14 | E-GEOD-6263 | biostudies-arrayexpress

Normal mouse skin lacking Hras

2015-03-01 | GSE60769 | GEO

Normal mouse skin lacking Hras

Project description:Oncogenic activating mutations in Ras genes are among the most common drivers of human disease. Treating mouse skin with the chemical carcinogen DMBA induces a characteristic mutation in Hras at codon 61. To understand how skin responds to a constitutive lack of Hras, we generated a cohort of Hras knockout mice. A backcross was generated using male Mus spretus and female FVB/N Hras-/- mice; female F1 hybrids were mated with male FVB/N Hras -/- or Hras -/+ mice to generate a backcross population. This series contains mice that were Hras -/-. Mice were aged to 8 weeks and a tail skin sample was snap frozen.

2015-03-01 | E-GEOD-60769 | biostudies-arrayexpress

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