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A conserved microRNA signature related to cellular transformation by the RAS oncogene (miRNA)

ABSTRACT: The differential expression of microRNAs in Ras transformed epithelial cells of human and rat origin was investigated. Here we describe the group of miRNAs differentially expressed in two Ras transformed cell lines and defined it as a miRNA Ras signatures. We show that expression of these miRNAs are also affected in different primary tumors with high frequency of Ras mutation. We demonstate that introduction of different miRNAs lost during Ras transformation have big influence on cellular phenotype and mRNA expression. Importance of Ras pathway dependent transcription factors for miRNA regulation was shown as well. The complexity of miRNA – signal transduction pathways interactions and importance of miRNA regulation in Ras dependent malignant tumor formation is discussed.

ORGANISM(S): Rattus norvegicus Homo sapiens

PROVIDER: GSE46794 | GEO | 2020/08/28

REPOSITORIES: GEO

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A conserved microRNA signature related to cellular transformation by the RAS oncogene (Affymetrix mRNA)

Project description:The differential expression of microRNAs in Ras transformed epithelial cells of human and rat origin was investigated. Here we describe the group of miRNAs differentially expressed in two Ras transformed cell lines and defined it as a miRNA Ras signatures. We show that expression of these miRNAs are also affected in different primary tumors with high frequency of Ras mutation. We demonstate that introduction of different miRNAs lost during Ras transformation have big influence on cellular phenotype and mRNA expression. Importance of Ras pathway dependent transcription factors for miRNA regulation was shown as well. The complexity of miRNA – signal transduction pathways interactions and importance of miRNA regulation in Ras dependent malignant tumor formation is discussed.

2020-08-28 | GSE46301 | GEO

Differential gene expression in Ki-RAS and Ha-RAS cell lines.

Project description:Comparison of gene expression in Ha-RAS transformed cells versus untransformed Caco-2. Comparison of gene expression in Ki-RAS transformed cells versus untransformed Caco-2.

2009-04-07 | GSE12203 | GEO

MicroRNA profiling of human HeLa cells overexpressing p19 H-Ras

Project description:MicroRNA miRNA expression profiles for human HeLa cells (Cervical cancer), overexpressing p19 H-Ras, were examined to investigate the miRNA regulation by p19 H-Ras. miRNA microarray analysis identified statistical unique profiles, which could discriminate miRNAs regulated by p19 H-Ras and not regulated by the p19 mutant (W164A) H-Ras.

2008-12-12 | E-TABM-494 | biostudies-arrayexpress

Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis

Project description:To gain insight into the differential signaling pathways triggered in N-RAS-/- versus N-RAS+/+ mice during liver injury and fibrosis, we performed microarray analyses of livers 28 days after CCl4 treatment and BDL surgery, respectively. Our findings suggested that increased cell proliferation and matrix deposition as well as loss of cell homeostasis were characteristic of N-RAS-/- after experimental fibrosis. We used microarrays to detail the global programme of gene expression underlying CCl4 and BDL challenge,

2023-07-15 | GSE236915 | GEO

Gene expression changes with inducible expression of activated ras and ras effector domain mutants

Project description:The goals of this study were to identify gene transcription changes in cells expressing activated H-RasV12 or activated versions of the ras effector domain mutants RasV12G37, RasV12S35, and RasV12C40 for the purpose of identifying common or unique transcription alterations in cells transformed by different ras signal transduction pathways. Keywords: genetic modification design

2008-08-01 | GSE8916 | GEO

Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

Project description:We performed tanscriptional profiling of ARPE19 and four isogenic transformed cells lines in which Ras or two downstream pathways, MAPK or PI3K/mTOR, were up-regulated. The purpose of this study is to understand how Ras signaling impacts kinetochore function.

2022-09-21 | GSE172512 | GEO

Methylation induced by the RAS oncogene

Project description:Silencing of gene expression by methylation of CpG islands in regulatory elements is frequently observed in cancer. However, an influence of the most common oncogenic signalling pathways onto DNA methylation has not yet been investigated thoroughly. To address this issue, we identified genes suppressed in HRAS-transformed rat fibroblasts but up-regulated after treatment with the demethylating agent 5-Aza-CdR and with the MEK1,2 inhibitor U0126. Analysis of gene expression by microarray and Northern blot analysis revealed the MEK/ERK target genes clusterin, Mmp2, Ppicap, syndecan 4, Timp2, Thbs1 to be repressed in the HRAS-transformed FE-8 cells in a MEK/ERK- and in a methylation-dependent manner. Hypermethylation of putative regulatory elements in HRAS-transformed cells as compared to immortalized fibroblasts was detected within a CpG island 14.5 kb upstream of clusterin, within the clusterin promoter and within a CpG island of the Mmp2 promoter by bisulphite sequencing. Furthermore, hypermethylation of the clusterin promoter was observed ten days after induction of HRAS in immortalized rat fibroblasts and a clear correlation between reduced clusterin expression and hypermethlyation could also be observed in distinct rat tissues. These results suggest that silencing of individual genes by DNA methylation is controlled by oncogenic signalling pathways, yet the mechanisms responsible for initial target gene suppression are variable. Keywords: expression analysis

2006-03-12 | GSE4427 | GEO

Wild type N-ras displays anti-malignant properties, in part by downregulating decorin

Project description:Previously, we have demonstrated that wild type N-ras (wt N-ras) harbors an anti-malignant effect against mutated Ras and in tumors without Ras mutations. To investigate the molecular bases of this anti-malignant activity, we have studied the potency of this anti-malignant effect in a model system against SV40 T. We show that wild-type N-ras (wt N-ras) counteracts the effects of SV40T in NIH3T3 cells as seen by a decrease in proliferation, anchorage independence and changes in migration). We also show that wt N-ras also elicits the same anti-malignant effects in some human tumor cell lines (HT1080 and MDA-MB-231). Through mRNA and microRNA (miRNAs) expression profiling we have identified genes and miRNAs modulated by wt N-ras potentially responsible for the anti-malignant effect. wt N-ras appears to mediate its anti-malignant effect by downregulating some of the targets of the TGFb pathway and decorin, which are able to reverse the inhibition of migration induced by wt N-ras. Our experiments show that the molecules that mediate the anti-malignant effect appear to be different than those modulated by transforming N-ras. The components of the pathways modulated by wt N-ras mediating its anti-malignant effects are potential targets for therapeutic intervention in cancer. We report that the N-ras proto-oncogene has anti-malignant effects and that it does so by modulating different genes than its oncogenic counterpart, which indicates that it should be activating different pathways. Gene expression profiles from 3T3 cells transformed by SV40 (SV5) and cells expressing both SV40T and wt N-ras (SV5-NN clones) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Mouse 430 2.0) and key targets were validated by real time RT-PCR.

2011-04-19 | E-GEOD-28678 | biostudies-arrayexpress

Oncogene Regulated Release of Extracellular Vesicles

Project description:Oncogenes can alter metabolism by changing the balance between anabolic and catabolic processes. However, how oncogenes regulate tumor cell biomass remains poorly understood. Using isogenic MCF10A cells transformed with nine different oncogenes, we show that specific oncogenes reduce the biomass of cancer cells by promoting EV release. While MYC and AURKB elicited the highest number of EVs, each oncogene selectively altered the protein composition of released EVs. Likewise, oncogenes alter secreted miRNAs. MYC overexpressing cells require ceramide, while AURKB require ESCRT to release high levels of EVs. We identify an inverse relationship between MYC upregulation and activation of the RAS/MEK/ERK signaling pathway for regulating EV release in some tumor cells. Finally, lysosome genes and activity are downregulated in the context of MYC and AURKB, suggesting that cellular contents instead of being degraded, were released via EVs. Thus, oncogene mediated biomass regulation via differential EV release is a new metabolic phenotype.

2021-04-16 | MSV000087219 | MassIVE

Proteomic analysis of 3D cultures of fibroblasts and Ras-transformed HaCaT keratinocytes

Project description:HaCaT, and its three retrovirally c-Ha-ras-transformed subclones, A5, II-4 and RT3 (abbreviated as ras-HaCaTs in the text) that exhibit benign, invasive and malignant phenotypes, respectively, were cultured as 3D monocultures and co-cultures with fibroblasts. After hypotonic lysis of the cells, the insoluble proteins were analysed by LC-MS/MS.

2019-09-10 | PXD013113 | Pride

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