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Effect of Omomyc treatment on lung adenocarcinoma of KRasLSL-G12D/+ transgenic mouse and human lung adenocarcinoma cell lines

ABSTRACT: Effect of Omomyc treatment on lung adenocarcinoma of KRasLSL-G12D/+ transgenic mouse and human lung adenocarcinoma cell lines

PROVIDER: PRJNA521962 | ENA |

REPOSITORIES: ENA

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

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

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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

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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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RNA seq analysis of primary tumors and metastases from the NPK (Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+; R26R-CAG-LSL-EYFP/+) prostate cancer mouse model

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Whole-exome sequencing analysis of primary tumors and metastases from the NPK (Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+; R26R-CAG-LSL-EYFP/+) prostate cancer mouse model

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