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CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer

ABSTRACT: CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer

PROVIDER: PRJNA471762 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7174660.fastq.gz	Fastqsanger.gz
	SRR7174661.fastq.gz	Fastqsanger.gz
	SRR7174662.fastq.gz	Fastqsanger.gz
	SRR7174663.fastq.gz	Fastqsanger.gz
	SRR7174664.fastq.gz	Fastqsanger.gz

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CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer

Project description:The study evaluated the differential gene expression in CBX5 knockdown cells compared to control shRNA expressed HCC827 cells. Briefly, human lung cancer HCC827 cells stably expressing either CBX5 shRNAs or control shRNA were analysed for gene expression.

2023-01-05 | GSE114563 | GEO

Splicing targeting approaches highlight actionable vulnerabilities in advanced prostate cancer [22Rv1]

Project description:To investigate if pharmacological inhibition of splicing could uncover novel actionable vulnerabilities in CRPC, we profiled the genome-wide transcriptional changes elicited in 22Rv1 cells by treatment with three drugs that inhibit the splicing through different molecular targets: i. Pladienolide B, that impairs the activity of SF3B1; ii. Indisulam that promote degradation of the splicing factor RBM39; iii. THZ531 inhibits the cyclin dependent kinases (CDK) 12 and 13.

2024-03-06 | GSE234734 | GEO

Splicing targeting approaches highlight actionable vulnerabilities in advanced prostate cancer [22Rv1]

Project description:Splicing targeting approaches highlight actionable vulnerabilities in advanced prostate cancer [22Rv1]

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Systematic analyses of RNA-binding proteins uncover therapeutically promising vulnerabilities in osteosarcoma

Project description:Systematic analyses of RNA-binding proteins uncover therapeutically promising vulnerabilities in osteosarcoma

| PRJNA1032883 | ENA

BRD4 represses CBX5

Project description:BRD4 is amplified and/or up-regiulated in a subset of ovarian cancer which correlates with a poor survival siRNA sensitization screens in the presence of CHK1 inhibitor, LY2606368, identify BRD4 as a therapeutic target in ovarian cancer. BRD4 suppression by either siRNA or using JQ1 increases CBX5 expression

2016-05-01 | GSE78704 | GEO

Decreased serine biosynthesis identifies a subgroup of platinum resistant ovarian cancers and novel actionable metabolic vulnerabilities

Project description:Decreased serine biosynthesis identifies a subgroup of platinum resistant ovarian cancers and novel actionable metabolic vulnerabilities

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Analysis of open chromatin structures in HCC827 CBX5 knockdown cells by ATAC seq analysis .

Project description:Briefly, Human lung cancer HCC827 cells were stably expressing either CBX5 shRNAs or control shRNA were analysed for open chromatin structures using ATAC seq Analysis.

2024-02-18 | GSE167071 | GEO

Maternal RNF114 plays critical roles in activation of the early zygotic genome through promoting ubiquitin-mediated degradation of Chromobox protein CBX5

Project description:Zygotic genomic activation (ZGA) is a landmark event in the maternal-to-zygotic transition (MZT), and the regulation of ZGA by maternal factors remains to be elucidated. In this study, the depletion of maternal RNF114 led to 2-cell embryos developmental arrest in mice. RNF114 was proven to play an important role in major ZGA using ethynyl uridine (EU) incorporation and transcriptome analysis. To study the underlying mechanism, we performed protein profiling in mature oocytes and found a potential substrate for RNF114, Chromobox protein CBX5, whose ubiquitination and degradation was regulated by RNF114. Furthermore, the overexpression of CBX5 prevented embryonic development and impeded major ZGA. In summary, our study reveals that maternal RNF114, as a ubiquitin E3 ligase, plays a precise role in mediating the degradation of repressive protein CBX5 during MZT, the misregulation of which may impede the appropriate activation of major ZGA in mouse embryos.

2021-06-16 | GSE164532 | GEO

Genomic profiling of biliary tract cancer cell lines reveals molecular subtypes and actionable drug targets

Project description:Purpose: Biliary tract cancers (BTCs) carry a very poor prognosis and have no approved targeted therapies. Recent genomic profiling of primary BTCs identified a number of potentially actionable drug targets, however accurate model systems to evaluate these targets are currently lacking. The purpose of this study was to compare the genomic landscape of commonly used BTC cell lines to primary BTCs, and to utilize these models for drug target evaluation. Design: Twenty BTC cell lines were profiled by RNA-seq analysis. Results: Transcriptomic profiling of BTC cell lines identified two subtypes, enriched for epithelial and mesenchymal genes respectively, which were also identified in primary BTC. Conclusions: Cell lines harbor similar genomic alterations to primary BTCs. Integration of cell line and primary cancer data identify novel molecular subsets, and highlight specific molecular vulnerabilities in BTC.

2019-10-12 | GSE138772 | GEO

Molecular and functional profiling identifies therapeutically targetable vulnerabilities in plasmablastic lymphoma.

Project description:Plasmablastic lymphoma (PBL) represents a rare and aggressive lymphoma subtype frequently associated with immunosuppression. Clinically, patients with PBL are characterized by poor outcome. The current understanding of the molecular pathogenesis is limited. A hallmark of PBL represents its plasmacytic differentiation with loss of B-cell markers and, in 60% of cases, its association with Epstein-Barr virus (EBV). Roughly 50% of PBLs harbor a MYC translocation. Here, we provide a comprehensive integrated genomic analysis using whole exome sequencing (WES) and genome-wide copy number determination in a large cohort of 96 primary PBL samples. We identify alterations activating the RAS-RAF, JAK-STAT, and NOTCH pathways as well as frequent high-level amplifications in MCL1 and IRF4. The functional impact of these alterations is assessed using an unbiased shRNA screen in a PBL model. These analyses identify the IRF4 and JAK-STAT pathways as promising molecular targets to improve outcome of PBL patients.

| S-EPMC8408158 | biostudies-literature

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