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RNA-seq of human neuroblastoma cell lines where RET is knocked out

ABSTRACT: RNA-seq of human neuroblastoma cell lines where RET is knocked out

PROVIDER: PRJEB42584 | ENA |

REPOSITORIES: ENA

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RNA-seq of human neuroblastoma cell lines where RET is knocked out

Project description:ALK is driving neuroblastoma (NB) and RET has been shown to be a downstream target of ALK signaling in NB. To get a better understanding of the role of RET in NB, the gene was knocked out in SKNAS cell lines.

2021-04-14 | E-MTAB-10032 | biostudies-arrayexpress

Loss of RET promotes mesenchymal identity in neuroblastoma cells

Project description:Aberrant activation of Anaplastic Lymphoma Kinase (ALK) drives neuroblastoma (NB). Previous work has identified the RET receptor tyrosine kinase (RTK) as a downstream target of ALK activity in NB models. We show here that ALK activation in response to ALKAL2 ligand results in the rapid phosphorylation of RET in NB cells, providing additional insight into the contribution of RET to the ALK driven gene signature in NB. To further address the role of RET in NB, RET knock-out (KO) SK-N-AS cells were generated by CRISPR/Cas9 genome engineering. Gene expression analysis of RET KO NB cells identified a reprogramming of NB cells to a mesenchymal (MES) phenotype that was characterized by increased migration and upregulation of the AXL and MET RTKs as well as integrins and extracellular matrix components. Strikingly, the upregulation of AXL in the absence of RET reflects the development timeline observed in the neural crest as progenitor cells undergo differentiation during embryonic development. Together, these findings suggest that a MES phenotype is promoted in mesenchymal NB cells in the absence of RET, reflective of a less differentiated developmental status.

2021-09-10 | PXD024551 | Pride

Neuroblastoma cell lines

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Quantitative Analysis of the Transcriptomes of Tyro3- overexpressed and knocked out cell lines

Project description:Quantitative Analysis of the Transcriptomes of Tyro3- overexpressed and knocked out cell lines

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Expression data from neuroblastoma of TH-MYCN/KI RetM919T mice

Project description:The RET gene has been identified previously as a target of activated ALK at the mRNA level in both human neuroblastoma cell lines and primary tumors as well as in murine tumors driven by mutated Alk and MYCN. Moreover, it has been shown that tumor growth of murine TH-MYCN/KI Alkmut tumors was impaired upon Ret inhibition by the vandetanib inhibitor, suggesting RET as a therapeutic target in ALK mutated neuroblastoma. To further demonstrate the crucial role of RET in ALK mutated driven neuroblastoma oncogenesis, transgenic TH-MYCN mice were bred with KI RetM919T tumors. We document an oncogenic cooperation between activated Ret and MYCN overexpression in neuroblastoma formation. We used microarrays to analyze the global programme of gene expression of MYCN/RetM919T tumors and compare these profiles with profiles of MYCN/Alkmut tumors (GSE46583). Altogether, our data show that MYCN/RetM919T tumors present with expression profiles close to MYCN/Alkmut tumors.

2017-09-15 | GSE72678 | GEO

Parkinson's disease-associated DJ-1 is required for the expression of GDNF receptor Ret in human neuroblastoma cells

Project description:DJ-1 is an atypical peroxiredoxin-like peroxidase that may act as a redox-dependent chaperone and a regulator of transcription. To explore DJ-1-mediated transcriptional control in Parkinsonâ??s disease (PD), we generated human neuroblastoma cells with inducible knock-down of DJ-1 expression. We then used functional genomic techniques to identify novel pathways dysregulated by loss of DJ-1 function. Using microarray gene expression profiling, we found that DJ-1 silencing alters the expression of 26 genes, with 10 down-regulated and 16 up-regulated transcripts. Among the down-regulated genes we found Ret, tyrosine kinase receptor for the neurotrophic factor GDNF. Taking advantage of Ingenuity Pathways Analysis, we identified hypoxia inducible factor 1 alpha (Hif1a) as a possible mediator of the interplay between DJ-1 and Ret. We show that Hif1a is stabilized in the absence of DJ-1, and that loss of DJ-1 generates hypoxia and accumulation of free radical species (ROS). Overexpression of wt DJ-1, but not of C106A and L166P mutants deficient in ROS scavenger activity, rescues Ret expression in neuroblastoma cells. These findings reveal novel players in PD pathogenesis and provide evidence for additional pathways involved in DJ-1-mediated neurodegeneration. Comparison between DJ-1-silenced human SH-SY5Y neuroblastoma cells and control cells. Two clones were selected for each condition, and each clone was analyzed in duplicate, for a total of 8 samples.

2010-04-28 | E-GEOD-17204 | biostudies-arrayexpress

Mechanistic insight into RET kinase inhibitors targeting the DFG-out conformation in RET-rearranged cancer

Project description:We used quantitative (phospho)proteomics to study how cells may escape the activity of RET kinase inhibitors.

2017-06-21 | PXD006006 | Pride

Genomic profile of IL10-/- knocked out colitis model

Project description:Objetives: study and characterization of the IL10-/- knocked out colitis model in mice at genomic level and the study of the influence of bacteria in the development of the disease. Keywords: Differentially expressed genes analysis

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Egg and liver proteome in vtg2 knocked-out zebrafish females

Project description:CRISPR/Cas9 knock-out of the vtg1 and vtg3 genes was performed in zebrafish separately. This project involves proteomics screening for validation of the absence of targeted proteins in vtg1 and vtg3 and their variants in knocked out female zebrafish in eggs and investigating possible changes within the corresponding proteomes as a results of the absence of these specific vitellogenins and their variants.

2023-10-09 | PXD042791 | Pride

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