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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)

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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

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

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.

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Impaired proteolysis of non-canonical RAS proteins drives clonal hematopoietic transformation [CRISPR]

Project description:Recently, screens for mediators of resistance to FLT3 and ABL kinase inhibitors in leukemia resulted in the discovery of LZTR1 as an adaptor of a Cullin-3 RING E3 ubiquitin ligase complex responsible for degradation of RAS GTPases. In parallel, dysregulated LZTR1 expression via aberrant splicing and mutations have been identified in clonal hematopoietic conditions. Here we identify that loss of LZTR1, or leukemia-associated mutants in the LZTR1 substrate and RAS GTPase RIT1 which escape degradation, drive hematopoietic stem cell expansion (HSC) and leukemia in vivo. LZTR1 null cells rely on multiple RAS GTPases for transformation. Consequently, RAS targeting bioPROTACs or reduction of GTP-loaded RAS overcomes LZTR1 loss-mediated resistance to FLT3 inhibitors. These data thereby reveal proteolysis of non-canonical RAS proteins as novel regulators of HSC function, define the function and spectrum of RIT1 and LZTR1 mutations in leukemia, and identify means to overcome drug resistance due to LZTR1 downregulation.

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

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