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Genome-wide analysis of tumor regression upon K-RAS inactivation

ABSTRACT: We performed expression profiling on micro-dissected lung tumors derived from a doxycycline-inducible K-RAS mouse model in order to gain mechanistic insight into K-RAS-mediated tumor maintenance. In this model, the tumors were induced with doxycycline for 11 weeks (in order to obtain lung tumors). At this point the doxycyline was withrawn from the food of the mice and consequently K-RAS inactivated. Thus, the genome-wide analysis was performed on tumors at timepoints 0, 24h and 48h after K-RAS inactivation.

ORGANISM(S): Mus musculus

PROVIDER: GSE40606 | GEO | 2012/09/06

SECONDARY ACCESSION(S): PRJNA174390

REPOSITORIES: GEO

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Genome-wide analysis of tumor regression upon K-RAS inactivation

Project description:We performed expression profiling on micro-dissected lung tumors derived from a doxycycline-inducible K-RAS mouse model in order to gain mechanistic insight into K-RAS-mediated tumor maintenance. In this model, the tumors were induced with doxycycline for 11 weeks (in order to obtain lung tumors). At this point the doxycyline was withrawn from the food of the mice and consequently K-RAS inactivated. Thus, the genome-wide analysis was performed on tumors at timepoints 0, 24h and 48h after K-RAS inactivation. Total RNA obtained from mouse lung tumors at time 0 and 24h or 48h after K-RAS inactivation.

2012-09-06 | E-GEOD-40606 | biostudies-arrayexpress

MicroRNA expression profiling of livers from the conditional doxycyline-regulatable c-Myc-driven liver tumor mouse model during tumor development and regression.

Project description:Progressing and regressing liver tumor tissues (depending on the group) were subjected to miRNA profiling to identify the miRNA changes occuring during tumor development and regression. Conditional doxycyline-regulatable c-Myc-driven mice get liver tumors following doxycycline (Dox) withdrawal from their diet. When mice are re-administered Dox through their diet, tumors start to regress.

2021-08-19 | GSE152920 | GEO

Gene expression profiling of Dox-activable K-ras mutation in human primary bronchial epithelial cell line

Project description:We constructed a primary lung cell model to permit regulated expression of KRASG12D. To do this, we leveraged a non-transformed, immortalized, human primary bronchial epithelial cell line (HBEC; hTert, CDK4, TP53 knockdown) that remains anchorage dependent and do not develop tumors when implanted into mice. We next modified these cells by stably integrating a regulatable KRASG12D allele, iKRASG12D, such that physiological expression of mutant KRAS is activated upon addition of doxycycline. The HBEC-iKRAS (WT) cell line and HBEC-iKRASG12D (MUT) cell line were propagated with or without Doxycycline (500ng/ml) respectively. RNA profiling of HBEC-iKRASG12D and HBEC-iKRASWT cells revealed widespread changes for HBECs harboring the activated KRAS allele in the presence of Dox. Within the KRASG12D-induced genes, the Molecular Signatures Database identified the oncogenic RAS signature as a top-enriched gene set. Upregulation of Ras signaling in Dox-treated HBEC-iKRASG12D cells was also supported by a significant overlap with a KRAS signature previously characterized by Singh et al.

2018-08-20 | GSE100336 | GEO

Gene regulation in ki-ras transfected murine fibroblasts

Project description:Ki-ras gene mutations are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, expression profiling analyses were performed using stable transfected NIH3T3 cells carrying different ki-ras gene mutations. Maybe, this analysis allows the discorvery of ras-associated cellular mechanisms, which might lead to the identification of physiological targets for pharmacological interventions of the treatment of Ki-ras-associated human tumors. Keywords: cDNA microarray, murine fibroblast, ki-ras mutations, carcinogenesis

2008-08-01 | GSE8372 | GEO

RNA-seq of human SH-EP neuroblastoma cell line with SOX11 overexpression as compared to control at 9h timepoint

Project description:RNA-seq to define downstream targets of adrenergic SOX11 upon 1ug/ml doxycyline inducible SOX11 overexpression in a SOX11 non-expressing mesenchymal cell line SH-EP. Analysis was performed 48h upon treatment with doxycycline, control samples are the untreated cells. 2 biological replicates were used.

2022-12-13 | E-MTAB-11892 | biostudies-arrayexpress

ATAC-seq of human SH-EP neuroblastoma cell line with SOX11 overexpression as compared to control

Project description:ATAC-seq to define open and closed chromatin in the human SH-EP neuroblastoma cell upon 1ug/ml doxycyline inducible SOX11 overexpression. Analysis was performed 48h upon treatment with doxycycline, control samples are the untreated cells. 3 biological replicates from different monoclonal expansions of SH-EP cells were used.

2023-12-30 | E-MTAB-11898 | biostudies-arrayexpress

Primary target of Fgf10 in embryonic mouse lung

Project description:We performed this experiment to identify the primary target of Fgf10 in lung development. We used a double transgenic system to either attenuate FGFR2b ligands Rosa26rtTAtet(O)solubleR2b based on the use of doxycycline we generated the samples after 6 and 9 hours of doxycyline induction, or to increase Fgf10 using Rosa26rtTAtet(O)fgf10 double transgenic system we generated samples after 9 of doxycycline induction, controls lungs are provided

2019-01-25 | GSE124154 | GEO

RNA-seq of human SH-EP neuroblastoma cell line with SOX11 overexpression as compared to control

2022-12-13 | E-MTAB-9338 | biostudies-arrayexpress

Gene regulation in ki-ras transfected murine fibroblasts

2010-05-25 | E-GEOD-8372 | biostudies-arrayexpress

Selective Requirement for Mediator MED23 in Ras-active Lung Cancer

Project description:K-RAS activating mutations occur frequently in non-small cell lung cancer (NSCLC), leading to aberrant activation of Ras-MAPK signaling pathway that contributes to the malignant phenotype. However, the development of Ras-targeted therapeutics remains challenging. Here, we show that MED23, a component of the multisubunit Mediator complex that is known to integrate signaling and gene activities, is selectively important for Ras-active lung cancer. By screening a large panel of human lung cancer cell lines with or without a Ras mutation, we found that Med23 RNAi specifically inhibits the proliferation and tumorigenicity of lung cancer cells with hyperactive Ras activity. Med23-deficiency in fibroblasts selectively inhibited the oncogenic transformation induced by Ras but not by c-Myc. Transcription factor ELK1, which is phosphorylated by MAPK for relaying the Ras signaling to MED23, was also required for the Ras-driven oncogenesis. Transcriptiome analysis revealed that MED23 and ELK1 co-regulate a common set of target genes enriched in regulating cell cycle and proliferation to support the Ras-dependency. Furthermore, correlated with the strength of Ras signaling as indicated by the ELK1 phosphorylation level, MED23 was up-regulated by Ras-transformation, and was found to be overexpressed in both Ras-mutated lung cancer cell lines and primary tumor samples. Remarkably, lower Med23 expression predicts better survival in Ras-active lung cancer patients and xenograft mice. Collectively, our findings demonstrate a critical role for MED23 in enabling the “Ras-addiction” of lung carcinogenesis, thus providing a vulnerable target for the treatment of Ras-active lung cancer. To gain a genome-wide understanding of how MED23 and ELK1 control gene expression in Ras-active lung cancer cells, we performed gene profiling experiments to analyze the transcriptomes from control, si-Med23, or si-Elk1 A549 cells.

2013-08-31 | GSE40517 | GEO

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