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Gene expression profiling of normal lung cells and K-RasG12V driven hyperplasias

ABSTRACT: We aimed to analyze the transcriptional profile of lung epithelial cells early after the expression of a resident K-RasG12V oncogene. This approach was based on the rationale that valuable therapeutic targets should be easier to detect in the first stages of tumor development due to tumor heterogeneity which occurr at late stages.

ORGANISM(S): Mus musculus

PROVIDER: GSE65256 | GEO | 2015/12/14

SECONDARY ACCESSION(S): PRJNA273511

REPOSITORIES: GEO

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Gene expression profiling of normal lung cells and K-RasG12V driven hyperplasias

Project description:We aimed to analyze the transcriptional profile of lung epithelial cells early after the expression of a resident K-RasG12V oncogene. This approach was based on the rationale that valuable therapeutic targets should be easier to detect in the first stages of tumor development due to tumor heterogeneity which occurr at late stages. We used a GEM model of lung adenocarcinoma driven by a resident K-RasG12V oncogene. In this GEM, the K-RasG12V allele also expresses a color marker that allows identification of K-RasG12V expressing cells at the single cell level in tissue sections. Thanks to this strategy we isolated early K-RasG12V-driven hyperplastic lesions (about 500 cells) and analyzed their gene expression profiling by Affymetrix GeneChip hybridization. Normal cells were isolated accordingly by LCM in the same lung sections.

2015-12-14 | E-GEOD-65256 | biostudies-arrayexpress

Gene expression profiling of advanced murine K-RasG12V lung adenocarcinomas

Project description:We aimed to analyze the transcriptional profile of full-blown murine lung adenocarcinomas driven by K-RasG12V oncogene. We used a GEM model of lung adenocarcinoma driven by a resident K-RasG12V oncogene. On average, tumors were collected 10 months after Adeno-CRE infection.

2015-12-14 | E-GEOD-65257 | biostudies-arrayexpress

Gene expression profiling of advanced murine K-RasG12V lung adenocarcinomas

Project description:We aimed to analyze the transcriptional profile of full-blown murine lung adenocarcinomas driven by K-RasG12V oncogene.

2015-12-14 | GSE65257 | GEO

Identification of differentially expressed genes between senescence and senescence bypass cells

Project description:We applied RNA-seq analysis to control and senescent human primary BJ fibroblast cells (senescence induced by activation of the oncogenic RASG12V gene), as well as in BJ cells that fully or partially bypass oncogene-idnuced senescence (OIS) due to knock-down of either p53 or BRD7 or LncRNA-OIS1 (using 4 different shRNAs).

2018-01-29 | GSE106414 | GEO

Gene Expression Analysis of Transgenic Myc-Driven Liver Tumor Formation and Regression

Project description:Gene expression changes were examined in transgenic MYC-driven liver cancers at different time points as tumors formed and upon early regression. Time points evaluated include: Control (non-tumor bearing), Pre-tumor (mice were removed from doxyclycine in their diet to induce MYC oncogene expression for 4-5 weeks), Tumor (tumor nodules from mice that had been off of doxycycline for 8-9 weeks) and Early tumor regression (tumor-bearing mice were placed back on doxycycline for 72 hrs to inhibit MYC oncogene expresion). MYC-Driven Mouse Tumor Models are described in Schahaf, et al., Nature, 2004 and Goga, et al., Nature Medicine, 2007. 11 Total Samples: 3 Control, 4 Pre-Tumor, 4 Tumor, 4 Early Tumor Regression. Control = LAP-tTA transgenic mice. Others = TRE-MYC x LAP-tTA double transgenic mice (doxy off).

2011-07-06 | E-GEOD-28198 | biostudies-arrayexpress

RNA-seq analysis of macrophages from normal and tumor-infiltrated omentum

Project description:Sequencing of mRNA from tissue-resident and tumor-associated macrophages in murine omentum display distinct transcriptional profile between macrophage subset of different origin

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Gene Expression Analysis of Transgenic Myc-Driven Liver Tumor Formation and Regression

2011-07-06 | GSE28198 | GEO

Functional CRISPR Screen Identifies AP1-associated Enhancer regulating FOXF1 to modulate Oncogene-Induced Senescence

Project description:We carried out CRISPR-Cas9 functional screen focused on AP-1 bound enhancers that are activated upon oncogenic stress. The screen discovered Enh.AP1.OIS1 - an enhancer bound by AP1 that is required for activation of oncogene-induced senescence (OIS) response. We applied RNA-seq analysis to RASG12V-activated BJ cells transduced with either sgRNAs targeting AP-1 bound enhancer (sgRNA-69 or sgRNA71), or sgRNA targeting the target gene FOXF1 or non-targeting control sgRNA (sgNT)

2018-07-15 | GSE112458 | GEO

Gene expression profile analysis of inducible melanotic and amelanotic melanoma in mice

Project description:We analyzed an inducible melanoma model in TiRP Ink4a/ArfF/F B10.D2 mice based on the conditional deletion in melanocytes of two tumor suppressor genes INK4a/Arf coupled to the expression of the oncogene H-rasG12V and a known tumor antigen (Hujibers et al. Cancer Res. 66:3278,2006; Soudja et al. Cancer Res. 70:3515-3525,2010). About 40% of these mice develop melanomas. Some tumors are heavily pigmented melanotic melanoma and grow slowly (hereafter referred to as “Mela”), but most of the induced tumors are nonpigmented amelanotic melanomas which are more aggressive (hereafter referred to as “Amela”). Gene expression profiles of the two types of tumors and of Amela-derived cell lines established in vitro were analyzed to identify the transcriptional signatures of these two types of tumors (including stromal components and infiltrating cells), as well as that intrinsic to Amela-tumor cells.

2013-06-26 | GSE29304 | GEO

Prolyl Isomerase PIN1 Modulates Oncogene Induced Senescence by Regulating PML-Nuclear Body Dynamics

Project description:Mammalian cells possess intrinsic mechanisms to prevent tumorigenesis upon deleterious mutations, including oncogene-induced senescence (OIS). The molecular mechanisms underlying OIS are, however, complex, and remain to be characterized. In this study, we analyzed the changes in the nuclear (phospho)proteome during the progression of OIS. Interestingly, we found that most of the phosphosites regulated during OIS were Prolyl Isomerase Pin1 targets. Our results show that Pin1 is a key regulator of several PML-NB proteins, specifically regulating several proteins upon oncogene activation. We have found that the constitutive PML-NB proteins are significantly regulated when PIN1 is depleted. Furthermore, we show that PIN1 knockdown promotes cell proliferation, while diminishing the senescence phenotype and hallmarks of senescence such as p21. Thus, our data provides preliminary evidence that PML-NB proteins are involved in regulating OIS via phosphorylation, and that the prolyl isomerase PIN1 acts as a tumor suppressor in response to oncogenic ER:RasG12V activation.

| MSV000090326 | MassIVE

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