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Cytosine methylation of mature microRNAs inhibits their functions and is associated with poor prognosis in glioblastoma multiforme

ABSTRACT: Cytosine methylation of mature microRNAs inhibits their functions and is associated with poor prognosis in glioblastoma multiforme

PROVIDER: PRJEB31319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3163230.fastq.gz	Fastqsanger.gz
	ERR3163225.fastq.gz	Fastqsanger.gz
	ERR3163226.fastq.gz	Fastqsanger.gz
	ERR3163227.fastq.gz	Fastqsanger.gz
	ERR3163228.fastq.gz	Fastqsanger.gz

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Cytosine methylation of mature microRNAs inhibits their functions and is associated with poor prognosis in glioblastoma multiforme.

Project description:BackgroundLiterature reports that mature microRNA (miRNA) can be methylated at adenosine, guanosine and cytosine. However, the molecular mechanisms involved in cytosine methylation of miRNAs have not yet been fully elucidated. Here we investigated the biological role and underlying mechanism of cytosine methylation in miRNAs in glioblastoma multiforme (GBM).MethodsRNA immunoprecipitation with the anti-5methylcytosine (5mC) antibody followed by Array, ELISA, dot blot, incorporation of a radio-labelled methyl group in miRNA, and miRNA bisulfite sequencing were perfomred to detect the cytosine methylation in mature miRNA. Cross-Linking immunoprecipiation qPCR, transfection with methylation/unmethylated mimic miRNA, luciferase promoter reporter plasmid, Biotin-tagged 3'UTR/mRNA or miRNA experiments and in vivo assays were used to investigate the role of methylated miRNAs. Finally, the prognostic value of methylated miRNAs was analyzed in a cohorte of GBM pateints.ResultsOur study reveals that a significant fraction of miRNAs contains 5mC. Cellular experiments show that DNMT3A/AGO4 methylated miRNAs at cytosine residues inhibit the formation of miRNA/mRNA duplex and leading to the loss of their repressive function towards gene expression. In vivo experiments show that cytosine-methylation of miRNA abolishes the tumor suppressor function of miRNA-181a-5p miRNA for example. Our study also reveals that cytosine-methylation of miRNA-181a-5p results is associated a poor prognosis in GBM patients.ConclusionTogether, our results indicate that the DNMT3A/AGO4-mediated cytosine methylation of miRNA negatively.

| S-EPMC7041276 | biostudies-literature

Cytosine methylation of mature microRNAs inhibits their functions and is associated with poor prognosis in glioblastoma multiforme

Project description:In the article we demonstrate that a significant fraction of mature microRNAs contains 5mC. We have developed a high-throughput bisulfite-based sequencing method to identify methylated microRNAs.

2020-12-31 | E-MTAB-7684 | biostudies-arrayexpress

Multiple myeloma immunoglobulin lambda translocations portend poor prognosis

Project description:Multiple myeloma immunoglobulin lambda translocations portend poor prognosis

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Distinct gene expression profile between ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis groups

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Distinct gene expression profile between ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis groups

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MYC regulation of a "poor prognosis" metastatic cancer cell state

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Multiple myeloma immunoglobulin lambda translocations portend poor prognosis

Project description:Multiple myeloma is a malignancy of antibody-secreting plasma cells. Most patients benefit from current therapies, however, 20% of patients relapse or die within two years. To better understand and identify these ‘high-risk’ cases, we analyzed the translocation landscape of myeloma from 795 newly-diagnosed patients by whole genome sequencing from the CoMMpass study. Translocations involving the immunoglobulin lambda (IgL) locus were identified in 10% of patients, and were indicative of poor prognosis. Importantly, 70% of IgL translocations co-occurred with hyperdiploid disease, a marker of standard risk, potentially resulting in the misclassification of IgL-translocated myeloma. Most IgL-translocations coincided with focal amplifications that were centered on the 3’ enhancer. Patients with IgL-translocations failed to benefit from immunomodulatory imide drugs (IMiDs), which target the lymphocyte-specific transcription factor IKZF1 that is bound to the IgL 3’ enhancer at some of the highest levels in the myeloma epigenome. These data implicate IgL-translocation as a driver of poor prognosis which may be due in part to IMID resistance.

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Comprehensive Homozygous Deletion Mapping of Myeloma Defines a Poor Prognosis Cell Death Gene Expression Signature

Project description:Myeloma is a clonal malignancy of plasma cells. Poor prognosis risk is currently identified by clinical and cytogenetic features. However, these indicators do not capture all prognostic information. Gene expression analysis can be used to identify poor prognosis patients and this can be improved by combination with information about DNA level changes. Using SNP-based gene mapping in combination with global gene expression analysis we have identified homozygous deletions in genes and networks that are relevant to myeloma. From these, we have generated an expression-based signature associated with shorter survival in 247 patients and confirmed this signature in data from 2 independent groups totalling 800 patients. We identified 170 genes with homozygous deletions and corresponding loss of expression. Deletion within the “Cell Death” network was over-represented and cases with these deletions have impaired overall survival. We defined a gene expression signature of 97 cell death genes that reflects prognosis confirmed this in two independent data sets. We developed a simple 6-gene expression signature from the 97-gene signature that can be used to identify poor prognosis myeloma in the clinical environment. The signature can form the basis of future trials aimed at improving the outcome of poor prognosis myeloma.

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CGGBP1 inhibits cytosine methylation at repetitive DNA sequences

Project description:By depleting CGGBP1 in normal human fibroblasts and by performing genome-wide sequencing (with and without bisulfite conversion) we show that upon CGGBP1 depletion cytosine methylation increases significantly at repeat regions. Using Pacbio sequencing of Alu and LINE-1 repeats amplified genome-wide from bisulfite converted DNA, we further establish the cytosine methylation-inhibitory functions of CGGBP1.

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