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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from lung tumor and stromal cells of KrasTgfbr2 -/- mouse model

ABSTRACT: 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 ul of saline containing 3x10e10 particles of an adenovirus containing the Cre recombinase (Ad.Cre) was administered to each LSL-KrasG12D mouse intra-nasally. We evaluated the tumor microenvironment response to Tgfbr2 deficient tumor cells. We compared lung tumor cell and stromal cell transcriptional profiles from five-week KrasTgfbr2 -/- and nine-week KrasTgfbr2 WT mice. We used mice at these time points to allow comparison of the stromal compartment of similarly advanced tumors.

ORGANISM(S): Mus musculus

SUBMITTER: Charles Powell

PROVIDER: E-GEOD-27675 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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. Mice were sacrificed at 7 weeks after administration of Adeno-Cre. We used laser capture microdissection to acquire tumor cells from KrasTgfbr2-/- and KrasTgfbr2 wt mouse tumors.

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

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

2011-09-15 | GSE27717 | GEO

Expression data from lung tumor and stromal cells 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 ul of saline containing 3x10e10 particles of an adenovirus containing the Cre recombinase (Ad.Cre) was administered to each LSL-KrasG12D mouse intra-nasally.

2011-09-15 | GSE27675 | GEO

Effect of vimentin deletion on gene expression in Kras-G12D-mutant, p53-null lung adenocarcinoma cells

Project description:Tumor initiation was induced in LSL-KrasG12D/+;Tp53flox/flox (KPV+/+) and LSL-KrasG12D/+;Tp53flox/flox;Vim-/- (KPV-/-) mice by Ad-cre delivery. Tumor cells were collected after 6 weeks and maintained in culture. RNA was collected from three independent cell lines per group and subjected to sequencing.

2023-05-31 | GSE225083 | GEO

Comparison of gene expression signatures between Cre- KTC organoid organoid and Cre+ KTC organoid

Project description:To identify downstream genes involved in cholangiocarcinoma development by genetic manipulations of Kras, TGFbR2, and CDH1, we cultured the biliary organoid from the extrahepatic bile duct of Cre-negative LSL-KrasG12D;Tgfbr2flox/flox;CDH1flox/flox (KTC) mice, and induced gene recombination using a lentivirus expressing Cre-recombinase (Cre+ KTC organoid) or control lentivirus (Cre- KTC organoid). Then, we compared gene expression signatures between Cre- KTC organoid organoid and Cre+ KTC organoid.

2017-04-30 | GSE88900 | GEO

Gene expression in lung cells expressing MycER/KrasG12D from a transgenic mouse model of non-small cell lung cancer

Project description:A transgenic mouse model of Kras-driven lung adenocarcinoma, with reversible activation of Myc, was used to explore the effect of Myc activity on lipid metabolism in lung tumours. Gene expression analysis links lipid metabolism, transport and storage to Myc activity. Lung cells from adeno-cre infected R26LSL-CMER and LSL-KrasG12D; R26LSL-CMER mice were isolated 14 days post-treatment with (LSL-KrasG12D; R26LSL-CMER and R26LSL-CMER) or without (R26LSL-CMER only) tamoxifen. GFP positive cells were FACs sorted. To increase RNA yield, cells from two mice of the same genotype and treatment were combined. There were two biological replicates for each condition. Gene expression was compared between lung cells with inactive MycER and lung cells expressing active MycER plus or minus KRasG12D.

2020-08-10 | E-MTAB-9131 | biostudies-arrayexpress

Glutaminase inhibition impairs CD8 T cell activation in STK11/Lkb1 deficient lung cancer

Project description:To characterize the impact of KRAS co-mutations KEAP1 and STK11/Lkb1 on the metabolic and immune microenvironment of lung adenocarcinoma in immune-intact models, we generated a cohort of genetically engineered mouse models (GEMMs) to reflect the diverse tumor suppressor landscape seen in patients. Mice carrying the KrasG12D allele (K)21 were crossed with Keap1flox/flox (KK)22 and/or Lkb1flox/flox (KKL, KL)23 mice and genetic recombination induced by intranasal inhalation of Ad5-CMV-Cre adenovirus. We interrogated the metabolites present in lung tumor nodules collected from cohorts of KK, KL and KKL mice.

2022-01-18 | ST002066 | MetabolomicsWorkbench

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

2019-06-30 | GSE132096 | GEO

Bone Marrow Derived Mesenchymal Stem Cells Incorporate Into the Prostate During Regrowth

Project description:Transcriptional profiling of mouse prostate stromal cells knocked out for Tgfbr2 were compared to that of the Tgfbr2-flox control. Elevated chemokine expression in the prostate stroma of a castrate resistant mouse model, Tgfbr2-fspKO, prompted us to determine the role of bone marrow derived cell recruitment to the prostate during regrowth. Tgfbr2-flox prostate epithelia vs. Tgfbr2-fspKO prostae epithelia. Biological replicates: 3 Tgfbr2-flox mouse prostates pooled, 3 Tgfbr2-fspKO mouse prostate replicates.

2010-06-16 | E-GEOD-22130 | biostudies-arrayexpress

BCL6 is regulated by the RAS/MAPK/ELK axis and promotes KRAS-driven lung cancers

Project description:Mutational activation of KRAS represents a common oncogenic event in lung cancers and still lacks effective treatments so far. Here, we identify the proto-oncogene B-cell lymphoma 6 (BCL6) as a lynchpin for KRAS dependence. BCL6 transcription was markedly promoted upon inducible activation of KRAS in either LSL-KrasG12D mice lung tumor tissue or engineered KRAS isogenic cell lines. Constitutive expression of BCL6 was also observed in patients with KRAS-mutant lung adenocarcinoma and associated with poor survival. Employing chemical and genetic screens, we characterized that the MAPK/ELK1 axis downstream of KRAS directly regulated BCL6 expression. Genetic depletion or pharmacological inhibitor targeting BCL6 preferentially impedes the proliferation of KRAS-mutant lung cancer cells by suppressing pre-RC protein expression in cycling cells, ultimately leading to stalled replication and DNA damage in vitro. Accordingly, targeted inhibition of BCL6 significantly reduced tumor burden and mortality in LSL-KrasG12D/+ and patient-derived lung cancer xenograft mouse models in vivo. Taken together, these findings reveal an oncogenic role of BCL6 in promoting KRAS-addicted lung cancers and define that BCL6 inhibition confers a targetable vulnerability for this kind of disease.

2022-10-19 | GSE189545 | GEO

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