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RBM10 Deficiency Promotes Brain Metastasis by Modulating Sphingolipid Metabolism in an Animal Model of EGFR Mutation Lung Adenocarcinoma

ABSTRACT: RBM10 Deficiency Promotes Brain Metastasis by Modulating Sphingolipid Metabolism in an Animal Model of EGFR Mutation Lung Adenocarcinoma

PROVIDER: PRJNA1181035 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31200173_1.fastq.gz	Fastqsanger.gz
	SRR31200173_2.fastq.gz	Fastqsanger.gz
	SRR31200174_1.fastq.gz	Fastqsanger.gz
	SRR31200174_2.fastq.gz	Fastqsanger.gz
	SRR31200175_1.fastq.gz	Fastqsanger.gz

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RBM10 Deficiency Promotes Brain Metastasis by Modulating Sphingolipid Metabolism in an Animal Model of EGFR Mutation Lung Adenocarcinoma

Project description:Brain metastasis significantly contributes to the failure of targeted therapy in patients with EGFR-mutated lung adenocarcinoma (LUAD). Reduced expression of RBM10 is associated with brain metastasis in these patients. However, the mechanism by which RBM10 affects brain metastasis in EGFR-mutated LUAD remains unclear. Previous studies reveal that RBM10 mutations lead to decreased expression and deregulated splicing at a subset of junctions, primarily through exon skipping.

2025-03-19 | GSE280915 | GEO

Inactivation of the splicing factor RBM10 limits EGFR targeted therapy response in EGFR mutant lung cancer

Project description:Oncogene-driven lung cancers such as those with activating mutations in the epidermal growth factor receptor (EGFR) often harbor additional co-occurring genetic alterations. The significance of most alterations co-occurring with mutant EGFR remains unclear. We report the impact of loss of the mRNA splicing factor RBM10 in human EGFR mutant lung cancer. RBM10 loss decreased EGFR inhibitor efficacy in patient-derived EGFR mutant tumor models. RBM10 regulated mRNA splicing of the mitochondrial apoptotic regulator Bcl-x. Genetic inactivation of RBM10 diminished EGFR inhibitor-mediated apoptosis by altering Bcl-x splicing, decreasing Bcl-xS (pro-apoptotic) and increasing Bcl-xL (anti-apoptotic) levels. Co-inhibition of Bcl-xL and mutant EGFR overcomes resistance induced by RBM10 loss. RBM10 loss was a biomarker of poor response to EGFR inhibitor treatment in clinical samples. Inactivation of the splicing factor RBM10 is a key co-occurring genetic alteration in EGFR mutant tumors that limits EGFR inhibitor efficacy and a potential biomarker of Bcl-xL inhibitor response.

2022-06-04 | GSE199240 | GEO

Inactivation of the splicing factor RBM10 limits EGFR targeted therapy response in EGFR mutant lung cancer

Project description:Inactivation of the splicing factor RBM10 limits EGFR targeted therapy response in EGFR mutant lung cancer

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RNA-seq of RBM10 in LUAD cell lines

Project description:RNA-seq in isogenic RBM10-proficient and RBM10-deficient cells derived from lung adenocarcinoma cell lines HCC827 (parental and RBM10 knockout; control siRNA and RBM10 siRNA) and NCI-H1299 (parental and RBM10 knockout).

2024-04-01 | E-MTAB-13617 | biostudies-arrayexpress

CRISPR-Cas9 RBM10 synthetic lethality screen

Project description:Genome-wide CRISPR-Cas9 knockout screen using TKOv1 sgRNA library was performed in isogenic RBM10-proficient and RBM10-deficient HCC827 cells.

2023-03-04 | E-MTAB-12724 | biostudies-arrayexpress

Global analysis of alternative splicing regulated by RBM10

Project description:RBM10 is an RNA binding protein that was identified as a component of spliceosome complex, suggesting its potential role in splicing regulation. However, the direct experimental evidence for this function has been lacking. Here we characterized in vivo RBM10-RNA interactions and investigated the role of RBM10 in splicing regulation at the global level. We observed significant RBM10-RNA interactions in the vicinity of splice sites and identified hundreds of splicing changes following perturbation of cellular RBM10 abundance. A RNA splicing map integrating the binding pattern and splicing profiles revealed a significant correlation between RBM10-enhanced exon skipping events and its binding close to the splicing sites of both upstream and downstream introns. Furthermore, we demonstrated the splicing defects in a patient carrying a RBM10 mutation. Overall, our data provided insights into the mechanistic model of RBM10-mediated splicing regulation and established genomic resources for future studies on its function in different pathophysiological contexts.

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Global analysis of alternative splicing regulated by RBM10

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RBM5 and RBM10

Project description:RBM5 and RBM10

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Characterization of RBM10 interactome in unchallenged and MK1775-treated cells

Project description:Mapping of RBM10-interactome using GFP-trap purification of EGFP-RBM10 expressed in HEK293T cells before and after WEE1 inhibition by MK1775. HEK293T expressing EGFP only or EGFP-RBM10 fusion (2 main isoforms) were left untreated or treated with 300nM MK1775 for 4 hours prior to GFP-trap enrichment and mass spectrometry analysis.

2024-07-16 | PXD040109 | Pride

Identification of RBM5 and RBM10-dependent splicing events in 293Flp-In cells.

Project description:RBM5 and RBM10 are RNA-binding proteins and splicing regulators. These two proteins are putative paralogs in mammalian cells, sharing common domain organization and extensive protein sequence similarity, but their RNA-binding preferences differ. We developed a sensitive system to identify splicing events regulated by RBM5 and/or RBM10, deleting all RBM5 alleles in 293Flp-In cells, and reducing the expression of RBM10, which is partially rescued by activation of a cryptic exon (CE) in one of the RBM10 alleles. RBM5 or RBM10 transgenes were then introduced in these RBM5-null, RBM10 mutant cells (RBM5-/-;RBM10-/CE), allowing controlled protein expression, induced with Doxycycline. Using this system we identify thousands of RBM5 and RBM10-regulated cassette exons, and note a substantial overlap between the two sets.

2024-03-08 | GSE240259 | GEO

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