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Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [ASOseries]

ABSTRACT: Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [ASOseries]

PROVIDER: PRJNA854198 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19903574_1.fastq.gz	Fastqsanger.gz
	SRR19903574_2.fastq.gz	Fastqsanger.gz
	SRR19903575_1.fastq.gz	Fastqsanger.gz
	SRR19903575_2.fastq.gz	Fastqsanger.gz
	SRR19903576_1.fastq.gz	Fastqsanger.gz

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Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities.

Project description:Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities.

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Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [CRISPRseries]

Project description:Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [CRISPRseries]

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Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [CRISPRseries]

Project description:Long noncoding RNAs (lncRNAs) are widely dysregulated in cancer, yet their functional roles in cellular disease hallmarks remain unclear. Here we employ pooled CRISPR deletion to perturb 831 lncRNAs detected in KRAS-mutant non-small cell lung cancer (NSCLC), and measure their contribution to proliferation, chemoresistance and migration across two cell backgrounds. Integrative analysis of this data outperforms conventional “dropout” screens in identifying cancer genes, while prioritising disease-relevant lncRNAs with pleiotropic and background-independent roles. Altogether 80 high-confidence oncogenic lncRNAs are active in NSCLC, the majority identified here for the first time, and which tend to be amplified and overexpressed in tumours. A follow-up antisense oligonucleotide (ASO) screen shortlisted two candidates, Cancer Hallmarks in Lung LncRNA 1 (CHiLL 1) and GCAWKR, whose knockdown consistently suppressed cancer hallmarks in a variety of two- and three-dimension tumour models. Molecular phenotyping reveals that CHiLL 1 and GCAWKR control cellular-level phenotypes via distinct transcriptional networks converging on common oncogenic pathways. In summary, this work reveals a multi-dimensional functional lncRNA landscape underlying NSCLC that contains potential therapeutic vulnerabilities.

2022-07-05 | GSE207228 | GEO

Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities [ASOseries]

2022-07-05 | GSE207227 | GEO

Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities.

Project description:Long noncoding RNAs (lncRNAs) are widely dysregulated in cancer, yet their functional roles in cancer hallmarks remain unclear. We employ pooled CRISPR deletion to perturb 831 lncRNAs detected in KRAS-mutant non-small cell lung cancer (NSCLC) and measure their contribution to proliferation, chemoresistance, and migration across two cell backgrounds. Integrative analysis of these data outperforms conventional "dropout" screens in identifying cancer genes while prioritizing disease-relevant lncRNAs with pleiotropic and background-independent roles. Altogether, 80 high-confidence oncogenic lncRNAs are active in NSCLC, which tend to be amplified and overexpressed in tumors. A follow-up antisense oligonucleotide (ASO) screen shortlisted two candidates, Cancer Hallmarks in Lung LncRNA 1 (CHiLL1) and GCAWKR, whose knockdown consistently suppressed cancer hallmarks in two- and three-dimension tumor models. Molecular phenotyping reveals that CHiLL1 and GCAWKR control cellular-level phenotypes via distinct transcriptional networks. This work reveals a multi-dimensional functional lncRNA landscape underlying NSCLC that contains potential therapeutic vulnerabilities.

| S-EPMC9903773 | biostudies-literature

Multi-hallmark long noncoding RNA maps reveal non-small cell lung cancer vulnerabilities.

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

2022-07-05 | GSE207229 | GEO

High-confidence Coding and Noncoding Transcriptome Maps

Project description:High-confidence Coding and Noncoding Transcriptome Maps

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Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal. 2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging. 3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases. 4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.

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The Project for High-Confidence Coding and Noncoding Transcriptome Maps

Project description:The Project for High-Confidence Coding and Noncoding Transcriptome Maps

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Large-scale multi-omic analysis identifies noncoding somatic driver mutations and nominates ZFP36L2 as a driver gene for pancreatic ductal adenocarcinoma

Project description:Background The identification and characterization of somatic cancer driver mutations in the noncoding genome remains challenging. Objective To broadly characterize noncoding driver mutations for pancreatic ductal adenocarcinoma (PDAC). Design Using mutation calls from whole-genome sequence (WGS) data in PDACs and genome-scale maps of accessible gene regulatory regions in normal- and tumor-derived pancreatic samples, we analyzed enrichment of noncoding mutations in gene regulatory regions relevant to normal- and tumor-derived pancreatic contexts. Functional follow up of potential driver mutations was performed using chromatin interaction analyses, massively parallel reporter assays (MPRA) and targeted analysis of selected noncoding somatic mutations. Results We first created genome-scale maps of accessible chromatin regions (ACRs) and histone modification marks (HMMs) in pancreatic cell lines and purified pancreatic acinar and duct cells. Integration with whole-genome mutation calls from 506 PDACs revealed 314 ACRs/HMMs significantly enriched with 3,614 noncoding somatic mutations (NCSMs). Chromatin interaction analysis identified 416 potential target genes and MPRA revealed 178 NCSMs impacting reporter activity (19.45% of those tested). Targeted luciferase validation confirmed negative effects on gene regulatory activity for NCSMs near ZFP36L2 and CDKN2A. For the former, CRISPR interference (CRISPRi) identified ZFP36L2 as a target gene (16.0 - 24.0% reduced expression, P = 0.023-0.0047), and growth inhibition after overexpression of ZFP36L2 (4.1 - 14.1-fold reduction, P = 6.0x10-4 - 3.2x10-3) implicates a possible tumor suppressor function. Conclusion Our integrative approach provides a catalog of potential noncoding driver mutations and nominates ZFP36L2 as a novel PDAC driver gene with a likely tumor suppressor function.

2025-07-23 | MSV000098624 | MassIVE

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