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Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation

ABSTRACT: Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation

PROVIDER: PRJNA545920 | ENA |

REPOSITORIES: ENA

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Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (miRNA expression)

Project description:Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (miRNA expression)

| PRJNA545940 | ENA

Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (mRNA expression)

Project description:Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (mRNA expression)

| PRJNA545941 | ENA

Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-30 | GSE132097 | GEO

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

Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (mRNA expression)

Project description:This experiment is designed to evaluate gene expression alteration and significant pathway(s) following HRasV12 transduction in BEAS-2B the immortalized human bronchial epithelial cell line, which causes senescence-like phenotype.

2019-06-30 | GSE132095 | GEO

The Wnt/β-catenin and RAS-ERK Pathways were Activated in Tissues of Chemotherapy-Resistant Gastric Cancer PDX Tumor

Project description:Chemotherapy resistance and disease recurrence remains major causes of gastric cancer patient mortality. We describe possible relationship between Wnt/b-catenin and RAS/ERK pathways in GC patients and acquired-resistant GC PDX tumors against FOLFOX, 5-fluorouracil-based chemotherapy. RNA sequencing analysis also demonstrates that Wnt/b-catenin pathway is an actionable target pathway for overcoming the chemotherapy resistance. These provide that an approach targeting both Wnt/b-catenin and RAS/ERK pathways could be novel therapeutic strategy in GC resistant to standard chemotherapy.

2019-05-26 | GSE128967 | GEO

Analyses of a deactivation genetic variation in Ha-Ras proto oncogene identified in a patient wit premature aging and insulin resistance

Project description:Inherited genetic variants of insulin receptor induced cellular signaling have long been suspected to contribute to the development of type-2- diabetes mellitus. In this report we discuss a heterozygous mutation in the first coding exon of the proto-oncogene Ha-Ras (Ha-RasA11P) that we have identified in a patient with familial premature aging syndrome. The patient has atopic sklerodermic skin alterations, insulin resistance as well as disturbances in lipid metabolism. In vitro analyzes have shown that this mutation disrupted not only the signal transduction of the insulin receptor but also other receptor tyrosine kinases, such as IGF-1, EGF, PDGF. These results demonstrate that HA-Ras has a significant role in insulin sensitivity in humans. We used microarrays to determine differences in gene expression due to a deactivating Ha-Ras mutation reducing c-fos expression in a patient with lipodystrophy and a Werner-like syndrome. Cultued fibroblasts of non diabetic controls and a patient with deactivating Ha-Ras mutation were analyzed at identical passage number and growth conditions without further additional treatment.

2013-08-07 | E-GEOD-49566 | biostudies-arrayexpress

Analyses of a deactivation genetic variation in Ha-Ras proto oncogene identified in a patient wit premature aging and insulin resistance

2013-08-07 | GSE49566 | GEO

Metabolic programs orchestrated by the activated Ha-ras and β-catenin oncoproteins in mouse liver tumors [mRNA]

Project description:The process of hepatocarcinogenesis in the diethylnitrosamine (DEN) initiation/phenobarbital (PB) promotion mouse model involves the selective clonal outgrowth of cells harboring oncogene mutations in Ha-ras, B-raf, or Ctnnb1. Here, we have characterized mouse liver tumors harboring either Ctnnb1 or Ha-ras mutations via integrated molecular profiling at the transcriptional and translational and post-translational levels. In addition, metabolites of the intermediary metabolism were quantified by high resultion 1H magic angle nuclear magnetic resonance (HR-MAS NMR). We have identified tumor characteristic genotype-specific differences in mRNA and miRNA expression, protein levels, and post-translational modifications and in metabolite levels that facilitate the molecular and biochemical stratification of tumor phenotypes. Bioinformatic integration of these data at the pathway level led to novel insights into tumor genotype-specific aberrant cell signaling and in particular to a better understanding of alterations in pathways of the cell intermediary metabolism, which are driven by the constitutive activation of the β-Catenin and Ha-ras oncoproteins in tumors of the two genotypes.

2014-02-10 | GSE51355 | GEO

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

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 | GSE46794 | GEO

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