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Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [RNA-Seq 22Rv1 M3 writing]

ABSTRACT: In this study, we used a targeted CRISPR/CasRx-METTL3 screen to identify m6A peaks that are critical for prostate cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE312888 | GEO | 2025/12/15

REPOSITORIES: GEO

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Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [CRISPR screen_H358]

Project description:In this study, we used a targeted CRISPR/CasRx-METTL3 screen to identify m6A peaks that are critical for prostate and lung cancer.

2025-12-15 | GSE312890 | GEO

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [CRISPR screen_22Rv1]

Project description:In this study, we used a targeted CRISPR/CasRx-METTL3 screen to identify m6A peaks that are critical for prostate and lung cancers.

2025-12-15 | GSE242446 | GEO

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [RNA-Seq 22Rv1 M3 writing]

Project description:Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [RNA-Seq 22Rv1 M3 writing]

| PRJNA1377563 | ENA

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer

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

2025-12-15 | GSE242447 | GEO

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [RNA-Seq_shKD]

Project description:To investigate the molecular role of CHD9 in prostate cancer, we knockdown CHD9 gene by two different shRNAs in 22Rv1 cells.

2025-12-15 | GSE242444 | GEO

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [ATAC-Seq]

Project description:To investigate the molecular role of CHD9 in prostate cancer, we knockdown CHD9 gene by two different shRNAs in 22Rv1 cells.

2025-12-15 | GSE255794 | GEO

Epitranscriptomic Editing Screening Identifies Functional m6A Sites in Cancer [ChIP-Seq]

Project description:To investigate the molecular role of CHD9 in prostate cancer, we knockdown CHD9 gene by two different shRNAs in 22Rv1 cells.

2025-12-15 | GSE255792 | GEO

Stage-specific requirement for Mettl3-dependent m6A epitranscriptomic regulation during myogenesis [RNA-Seq]

Project description:The role of N6-methyladenosine (m6A) in muscle formation and maintenance remains incompletely understood, particularly with respect to the contribution of methyltransferase-like 3 (METTL3), the core component of the methyltransferase complex (MTC), to myogenesis. Here, we show the involvement of METTL3 in the m6A epitranscriptome during myogenesis. Our findings reveal a correlation between METTL3-regulated m6A modifications and myoblast fusion during differentiation and regeneration. We observed significant upregulation of METTL3 following injury and identified numerous alterations in myogenic pathways. Furthermore, we detected differential patterns of METTL3-regulated m6A modifications in genes during differentiation, with some genes exhibiting loss and others showing gain. Our study revealed that the fusion factors Mymx and Mymk are downstream elements of METTL3 involved in myogenesis, and both exhibit upregulated expression and m6A levels during myogenesis. Our findings provide valuable resources for elucidating the function and mechanism of METTL3-regulated m6A modifications in myogenesis, thereby revealing the regulatory role of METTL3 in myoblast fusion.

2025-09-03 | GSE293208 | GEO

Stage-specific requirement for Mettl3-dependent m6A epitranscriptomic regulation during myogenesis [meRIP-Seq]

2025-09-03 | GSE293212 | GEO

Identifying the potential targets of METTL3 in macrophages by high-throughput m6A-seq

Project description:N6-methyladenosine (m6A), the most prevalent internal messenger RNA modification, plays critical roles in diverse biological processes. To characterize the potential involvement of METTL3 in macrophage function, we mapped m6A methylomes of METTL3-deficent and WT macrophages by m6A sequencing (m6A-seq) and RNA-seq, with independent biological replicates. Notably, among the m6A peaks with remarkable changes upon METTL3-depletion, the vast majority exhibited a significant (p < 0.05) decrease in m6A abundance.The most common m6A motif GGAC is significantly enriched in the m6A peaks in both WT and METTL3-deficent cells. A similar pattern of total and common m6A distribution in control and METTL3-deficient cells was observed, when the m6A peaks were especially abundant in the vicinity of CDS and 3’UTR regions.

2023-10-06 | GSE193340 | GEO

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