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Alteration of miRNA profiles between lung tumours from the KRASLSL-G12D/+ mice and the normal lung tissues

ABSTRACT: Alteration of miRNA profiles between lung tumours from the KRASLSL-G12D/+ mice and the normal lung tissues

PROVIDER: PRJNA909821 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22570327.fastq.gz	Fastqsanger.gz
	SRR22570328.fastq.gz	Fastqsanger.gz
	SRR22570329.fastq.gz	Fastqsanger.gz
	SRR22570330.fastq.gz	Fastqsanger.gz
	SRR22570331.fastq.gz	Fastqsanger.gz

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Alteration of miRNA profiles between lung tumours from the KRASLSL-G12D/+ mice and the normal lung tissues

Project description:Small RNA deep sequencing to determine the alteration of miRNA profiles in the lung tumours from the KRASLSL-G12D/+ mice compared with the normal lung tissues from the mice without Adeno-Cre treatment.

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mRNA transcriptome sequencing of CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Tp53fl/fl and KrasLSL-G12D/+Tp53fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre

Project description:Comparative gene expression profiling analysis of RNA-seq data in CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Tp53fl/fl and KrasLSL-G12D/+Tp53fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre.

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mRNA transcriptome sequencing of CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Lkb1fl/fl and KrasLSL-G12D/+Lkb1fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre

Project description:Comparative gene expression profiling analysis of RNA-seq data in CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Lkb1fl/fl and KrasLSL-G12D/+Lkb1fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre.

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Effect of Omomyc in vivo treatment on lung adenocarcinoma of KRasLSL-G12D/+ transgenic mouse

Project description:Analysis of Kras-driven lung adenocarcinoma of mice intranasally treated with 2.37 mg/kg Omomyc or vehicle (10 mM sodium acetate pH 6.5) for three days. KRasLSL-G12D/+ mice were treated with Omomyc by intranasal administration sixteen weeks after Adeno-Cre infection. Mice (n=2 for vehicle treated and n=3 for Omomyc treated group) were euthanized three days post-treatment and lung tumors were excised and frozen at -80ºC until processing.

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Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

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Gene expression differences between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice

Project description:Constitutive Kras and NF-kappaB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). However, the mechanisms of constitutive NF-kappaB activation in KrasG12D-induced PDAC are not yet understood. Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kappaB activation and completely suppressed PDAC development in KrasG12D and KrasG12D;Ink4a/Arf mutant mice, demonstrating a genetic link between IKK2/beta and KrasG12D in PDAC inception. Our findings reveal that KrasG12D-activated AP-1 induces IL-1alpha, which in turn activates NF-kappaB and its target genes IL-1alpha and p62, to initiate IL-1alpha/p62 feedforward loops for inducing and sustaining NF-kappaB activity. Furthermore, IL-1alpha overexpression correlates with Kras mutation, constitutive NF-kappaB activity, and poor survival in PDAC patients. Therefore, our findings establish a pathway linking duel feedforward loops of IL-1alpha/p62 through which IKK2/beta/NF-kappaB is activated by KrasG12D. To study Kras-induced inflammatory responses and to identify differentially expressed genes between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice, cDNA microarray analysis was performed.

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Project description:Effect of Omomyc in vivo treatment on lung adenocarcinoma of KRasLSL-G12D/+ transgenic mouse

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Comparison of KrasG12D/WT;p53Fx/Fx and KrasG12D/G12D;p53Fx/Fx MEFs

Project description:Microarray expression data generated to compare the biological impact of KrasG12D allelic duplication in p53null mouse embryonic fibroblasts (MEFs). The RAS/MAPK-signalling pathway is frequently deregulated in non-small cell lung cancer (NSCLC), often through activating mutations in KRAS. Mouse models demonstrated that activation of a single endogenous mutant Kras allele is sufficient to promote lung tumour formation, but acquisition of other genetic alterations is required for malignant progression. Using a well-established lung cancer mouse model we recently demonstrated that advanced KrasG12D-driven spontaneous tumours frequently exhibit enhanced MAPK signalling and KrasG12D allelic enrichment (KrasG12D/Kraswild-type>1), implying that mutant Kras copy gains are positively selected during lung cancer progression. To compare the oncogenic impact of a single mutant allele versus additional mutant Kras copy gain, we carried out a comprehensive analysis of mutant Kras homozygous and heterozygous MEFs and lung cancer cells and show that these genotypes are phenotypically distinct. Title: Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities Authors: Emma M Kerr, Edoardo Gaude, Frances K Turrell, Christian Frezza and Carla P Martins For MEF generation, KrasLSL-G12D/+ ;p53Fx/Fx mixed background (C57Bl/6/129/Sv) animals were interbred and embryos collected at day E12.5 to overcome KrasLSL-G12D/G12D embryonic lethality and Cre-mediated recombination performed immediately after MEF generation. Cells were cultured in DMEM supplemented with 10% FBS, 2 mM L-Glutamine for one passage and then infected with adenovirus-Cre (5âÃâ107âplaque-forming units/1 x 106 cells). Recombination of LoxP sites was confirmed by PCR analysis. Three independent embryos per genotype were analysed using GPL6887 Illumina MouseWG-6 v2.0 expression beadchip.

2016-02-24 | E-GEOD-75871 | biostudies-arrayexpress

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