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

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

PROVIDER: PRJNA198656 | ENA |

REPOSITORIES: ENA

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

Project description:A conserved microRNA signature related to cellular transformation by the RAS oncogene

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

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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.

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

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

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

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Gene expression changes induced by K-ras oncogene in the human pancreatic duct epithelial cell line (H6c7)

Project description:k-ras oncogene was transduced into the HPV16-E6E7 immortalized normal human pancreatic duct epithelial cell line (H6c7) to generate a stable K-ras oncogene-expressing cell line (H6c7-Kr). The gene expression profile of the H6c7-Kr cells was compared to that of H6c7 cells. We have excluded (subtracted) genes that were deregulated by transduction of the construct used for K-ras oncogene expression. Keywords: parallel sample

2005-01-11 | GSE1955 | GEO

Transcription profiling of human pancreatic duct epithelial cell line (H6c7) Gene expression changes induced by K-ras oncogene in the

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RAS-induced transformation of mammary epithelial cells relies on ZEB1-dependent cellular reprogramming through a paracrine process

Project description:The distinct frequency of activation of the RAS/MAPK signaling pathway in human cancers suggests a context-dependent cellular state of vulnerability to RAS transformation. While uncommon in breast cancers, oncogenic activation of this pathway is frequent in claudin-low (CL) tumors, a subtype of breast malignancies enriched in features of epithelial-mesenchymal transition (EMT), suggesting an interplay between RAS activation and EMT. Using inducible models of human mammary epithelial cells, we show that RAS-mediated transformation relies upon cellular reprogramming governed by the EMT-inducing transcription factor ZEB1. The path to ZEB1 induction involves a paracrine process: cells entering a senescent state following RAS induction release proinflammatory cytokines, notably IL-6 and IL1 which promote ZEB1 expression and activity in neighboring cells, thereby fostering their malignant transformation. Collectively, our findings unveil a previously unprecedented role for senescence in bridging RAS activation and EMT over the course of malignant transformation of human mammary epithelial cells.

2024-02-16 | GSE201536 | GEO

Transcriptional targets of oncogenic RAS proteins that mediate their ability to induce cellular transformation

Project description:Mutations in the NRAS oncogene are present in up to 20% of melanoma. Here, we show that interferon alpha-inducible protein 6 (IFI6) is necessary for NRASQ61K-induced transformation and melanoma growth. IFI6 was transcriptionally upregulated by NRASQ61K, and knockdown of IFI6 resulted in DNA replication stress due to dysregulated DNA replication via E2F2. This stress consequentially inhibited cellular transformation and melanoma growth via senescence or apoptosis induction depending on the RB and p53 pathway status of the cells. NRAS-mutant melanoma were significantly more resistant to the cytotoxic effects of DNA replication stress-inducing drugs, and knockdown of IFI6 increased sensitivity to these drugs. Pharmacological inhibition of IFI6 expression by the MEK inhibitor trametinib, when combined with DNA replication stress-inducing drugs, blocked NRAS-mutant melanoma growth. Collectively, we demonstrate that IFI6, via E2F2 regulates DNA replication and melanoma development and growth, and this pathway can be pharmacologically targeted to inhibit NRAS-mutant melanoma. MEL-ST cells expressing either empty vector or mutant oncogenic RAS genes (HRAS v12, KRAS v12, NRAS Q61K) were used to isolate total RNA. The RNA was then used to perform gene expression analyses using the Illumina HumanHT-12 V4.0 Expression BeadChip array.

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

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2022-07-17 | GSE190857 | GEO

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