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GLIOBLASTOMAS ARE CHARACTERIZED BY A REDUCED NUMBER OF M6A SITES IN LNCRNAs

ABSTRACT: GLIOBLASTOMAS ARE CHARACTERIZED BY A REDUCED NUMBER OF M6A SITES IN LNCRNAs

PROVIDER: PRJNA1189527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31451017_1.fastq.gz	Fastqsanger.gz
	SRR31451018_1.fastq.gz	Fastqsanger.gz
	SRR31451019_1.fastq.gz	Fastqsanger.gz
	SRR31451020_1.fastq.gz	Fastqsanger.gz
	SRR31451021_1.fastq.gz	Fastqsanger.gz

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GLIOBLASTOMAS ARE CHARACTERIZED BY A REDUCED NUMBER OF M6A SITES IN LNCRNAs

Project description:Recent studies have suggested the potential role of posttranscriptional N6-methyladenosine (m6A) RNA modifications in diverse biological processes, including tumor development. In contrast to intensively studied mRNA modifications, insufficient information is known so far about the epitranscriptome of long non-coding RNAs (lncRNAs). Furthermore, an epitranscriptome of LncRNAs in glioma pathogenesis has not been previously presented. Thus, this study aimed to profile m6A modifications within lncRNAs in different grades of gliomas using direct RNA long-read sequencing, with the goal of yielding both nucleotide and transcript-resolved m6A hits as biomarkers for tumor progression. Here we explored ONT direct RNA-seq to detect N6-methyladenosine (m6A) sites within lncRNAs' RRACH motifs in 26 glioma tumor tissues. Generally, 98.5% of m6A-modified RRACH motifs were detected in mRNA transcripts, and 1.16% in lncRNAs. We identified 60-748 unique m6A-modified lncRNAs for individual gliomas. On average, 15.84% of all RRACH motifs within lncRNAs were modified in glioblastomas (GB), while the m6A frequency reached 23.73% in the low-grade glioma (LGG) group. Unsupervised clustering analysis based on lncRNAs' m6A status resulted in three m6A clusters. Patients within the highly modified lncRNAs cluster (C3) experienced significantly longer survival compared to patients with lower methylation rates who were clustered into C1/C2 (2901 days in C3 vs 439 days in C1, log-rank test p=0.019).  In summary, we discovered that lncRNAs are highly modified in LGG while multiple epi-marks, found in low-grade gliomas, are absent in GB tissues revealing m6A contribution to glioma pathology.

2025-05-20 | GSE282642 | GEO

Prevalence of Copy-number neutral LOH in glioblastomas revealed by analysis of laser-microdissected tissues

2009-03-01 | GSE10922 | GEO

Prevalence of Copy-number neutral LOH in glioblastomas revealed by analysis of laser-microdissected tissues

Project description:We have employed a laser capture microdissection technique and single nucleotide polymorphism arrays to characterize genomic alterations associated with the development of glioblastomas. Combined analysis of LOH and copy number revealed that more than half of the identified 254 LOH loci showed no copy number alteration, indicating the presence of copy-number neutral LOH Keywords: DNA copy number, Loss of heterozygosity Affymetrix 50K SNP mapping arrays were used to profile 14 primary glioblastomas (GBMs) with matched blood DNA samples. Loss of heterozygosity (LOH) and copy number abnormality (CNA) profiles were derived from each tumour-blood pair.

2009-03-01 | E-GEOD-10922 | biostudies-arrayexpress

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Genome-wide gain-of-function screening characterized lncRNAs as tumor immune response regulators

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Genome-wide gain-of-function screening characterized lncRNAs as tumor immune response regulators [CRISPR_screen]

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Genome-wide gain-of-function screening characterized lncRNAs as tumor immune response regulators [CRISPR_screen]

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Genotyping by array of 123 IDH WT glioblastomas

Project description:Glioblastoma (GBM) is the most frequent and most aggressive form of diffuse glioma. The prognosis is very poor, with a median overall survival of 15 months after maximum safe resection and radiochemotherapy.GBM is one of the most genetically unstable cancers. It is characterized by numerous chromosome (chr) copy number alterations (CNA), such as chr 7 gain, chr 9p loss, and chr 10 loss, along with CDKN2A homozygous deletion (chr 9p21) and EGFR amplification (chr 7p11).Chromosome instability (CIN) may be the cause or the consequence of GBM development. In high-grade diffuse gliomas (HGG), CIN may initiate tumorigenesis. To identify recurrent genomic abnormalities in IDH WT glioblastomas, SNP arrays (Illumina 850K CytoSNP) were analyzed for 123 IDH WT GBM cases.

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