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MiRNA-Seq of MEF cells with or without Fbxw7 knock out

ABSTRACT: This study describes the transcriptome profiling of MEF cells with or without Fbxw7 knock out

ORGANISM(S): Mus musculus

PROVIDER: GSE164136 | GEO | 2023/12/30

REPOSITORIES: GEO

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Transcriptome of MEF cells with or without Fbxw7 knock out

Project description:This study describes the transcriptome profiling of MEF cells with or without Fbxw7 knock out

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Genome-wide distribution of MLL4, H3K4me1 and H3K4me3 in MEF cells

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MLL4, H3K4me1 and H3K4me3 Cut&Run in MEF cells; transcriptome of MEF cells with or without Fbxw7 knock out

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

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Transcriptome of EB differentiation at day 9th with or without PRDM16 or PR domain knock out [RNA-seq]

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FBXW7

Project description:Purpose: FBXW7 is one of the most frequently mutated tumor suppressors, the deficiency of which has been associated with resistance to some anticancer therapies. Through bioinformatic analyses and genome-wide CRISPR screens, we here reveal that FBXW7 deficiency leads to multi-drug resistance (MDR), to a bigger extent than well-established MDR-drivers such as ABCB1. Proteomic data from FBXW7-deficient cells and human cancer samples identify the upregulation of mitochondrial function as a hallmark of FBXW7 deficiency, which has been previously linked to an increased resistance to chemotherapy. Accordingly, genetic or chemical targeting of mitochondria is preferentially toxic for FBXW7-deficient cells. For instance, targeting mitochondrial translation with the antibiotic Tigecycline efficiently kills FBXW7-deficient cells in vitro and in vivo, by a mechanism that involves activation of the Integrated Stress Response (ISR). Searching for additional drugs that overcome MDR in FBXW7-deficient cells, we found several targeted therapies such as Erlotinib, Dasatinib or Vemurafenib which unexpectedly also activate the ISR. Together, our study reveals that one of the most frequent mutations in cancer reduces the sensitivity to the vast majority of available therapies, and identifies a general principle to overcome such resistance. Methods: This study was performed in 2 groups of DLD1 cells with duplicate samples per group. Both control (Wild Type, WT) and experimental (FBXW7 -/-, KO) were exposed to Tigecycline (10µM). DMSO was used as a control for the treatment. After 24h, the RNA was extracted and the transcriptome was profiled with RNA-Sequencing (RNA-seq) analysis. Results: our study reveals that one of the most frequent mutations in cancer reduces the sensitivity to the vast majority of available therapies, and identifies a general principle to overcome such resistance.

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Changes in global gene expression in SIN1 knock-out murine epithelial fibroblasts

Project description:RNA from wt and SIN1 knock-out MEF cell lines were compared Using affymetrix murine gene chip, the effects of SIN1 ablation on global gene transcription were assessed

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Effect of FBXW7 loss and concomitant FBXW7-KMT2D loss on mRNA levels

Project description:We assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. This experiment assesses the role of the FBXW7-KMT2D axis in regulating gene expression in OPM-1 cells.

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FBXW7 is a defining driver of uterine carcinosarcoma by promoting epithelial-mesenchymal transition

Project description:Fbxw7 is a tumor supressor frequently mutated in endometrial cancer. To analyze the signaling pathways that can be altered by Fbxw7 we compared RNA expression in the presence or absence of Fbxw7 in mouse endometrial cancer cells deficient for Fbxw7 and Pten.

2019-11-11 | GSE138490 | GEO

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