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An alternatively spliced variant of METTL3 mediates tumor suppression in hepatocellular carcinoma

ABSTRACT: An alternatively spliced variant of METTL3 mediates tumor suppression in hepatocellular carcinoma

PROVIDER: PRJNA782673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17012160_1.fastq.gz	Fastqsanger.gz
	SRR17012160_2.fastq.gz	Fastqsanger.gz
	SRR17012161_1.fastq.gz	Fastqsanger.gz
	SRR17012161_2.fastq.gz	Fastqsanger.gz
	SRR17012162_1.fastq.gz	Fastqsanger.gz

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An alternatively spliced variant of METTL3 mediates tumor suppression in hepatocellular carcinoma

Project description:Many steps of post-transcriptional mRNA processing have shown crucial roles in the tumorigenesis and progression of cancers, such as the N6-methyladenosine (m6A) modification and alternative splicing. Up-regulation of METTL3, the catalytic core of the m6A methyltransferase complex, increases the m6A levels and results in significant effects on the progression of hepatocellular carcinoma (HCC). However, alternative splicing of METTL3 has not been fully investigated and functions of its splice variants remain unclear. Here, we first analyze online and our transcriptomic data and obtain 13 splice variants of METTL3 besides the canonical full-length METTL3-A in HCC cell lines and tissues. Validated by RT-qPCR, we find that METTL3-D, one of the splice variants expressing a truncated METTL3 protein, exhibits higher levels than the METTL3-A in normal human livers but lower levels in HCC tumor tissues and cell lines. Further functional assays demonstrate that expression of METTL3-D decreases the cellular m6A modification, inhibits the proliferation, migration and invasion of HCC cells, and is negatively associated with the malignancy of patient tumors, exhibiting an opposite function as the full-length METTL3-A does. Analyses of TCGA data also show that HCC patients with higher levels of METTL3-D have longer survivals. This study demonstrates that the METTL3-D splice variant is a tumor suppressor, and it could be used as a potential target for the therapy of HCC.

2022-05-01 | GSE189372 | GEO

An Alternatively Spliced Variant of METTL3 Mediates Tumor Suppression in Hepatocellular Carcinoma.

Project description:Many post-transcriptional mRNA processing steps play crucial roles in tumorigenesis and the progression of cancers, such as N6-methyladenosine (m6A) modification and alternative splicing. Upregulation of methyltransferase-like 3 (METTL3), the catalytic core of the m6A methyltransferase complex, increases m6A levels and results in significant effects on the progression of hepatocellular carcinoma (HCC). However, alternative splicing of METTL3 has not been fully investigated, and the functions of its splice variants remain unclear. Here, we analyzed both our and online transcriptomic data, obtaining 13 splice variants of METTL3 in addition to canonical full-length METTL3-A in HCC cell lines and tissues. Validated by RT-qPCR and Western blotting, we found that METTL3-D, one of the splice variants expressing a truncated METTL3 protein, exhibits higher levels than METTL3-A in normal human livers but lower levels than METTL3-A in HCC tumor tissues and cell lines. Further functional assays demonstrated that METTL3-D expression decreased cellular m6A modification, inhibited the proliferation, migration, and invasion of HCC cells, and was negatively associated with the malignancy of patient tumors, exhibiting functions opposite to those of full-length METTL3-A. This study demonstrates that the METTL3-D splice variant is a tumor suppressor that could potentially be used as a target for HCC therapy.

| S-EPMC9031889 | biostudies-literature

Glycine max Alternatively Spliced Transcript Detecting Microarray (GmASDM).

Project description:Glycine max Alternatively Spliced Transcript Detecting Microarray (GmASDM).

| PRJNA643563 | ENA

Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

Project description:Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

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An alternatively spliced p62 isoform promotes breast cancer chemoresistance

Project description:An alternatively spliced p62 isoform promotes breast cancer chemoresistance

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Mutations primarily alter the inclusion of alternatively spliced exons

Project description:Mutations primarily alter the inclusion of alternatively spliced exons

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Mutations primarily alter the inclusion of alternatively spliced exons

Project description:Systematic mutagenesis has revealed that synonymous, non-synonymous and intronic mutations frequently alter the inclusion levels of alternatively spliced exons, suggesting that altered splicing might be a common mechanism by which mutations cause disease. However, most exons expressed in any cell are highly-included in mature mRNAs. Here, by performing deep mutagenesis of highly-included exons and by analysing the association between sequence variation and exon inclusion across the genome, we report that mutations only very rarely alter the inclusion of highly-included exons. This is true for both exonic and intronic mutations as well as for perturbations in trans. Therefore, mutations that affect splicing are not evenly distributed across the genome but are focussed in and around alternatively spliced exons with intermediate inclusion levels. These results provide a resource for prioritising synonymous and other variants as disease-causing mutations.

2020-06-29 | GSE151942 | GEO

Gene expression profiling of Capan-1 and Pt45P1 cells treated or not with alternatively spliced tissue factor (asTF)

Project description:The effects of alternatively spliced tissue factor (asTF) were measured by gene expression profiling of Capan-1 and Pt45P1 cells.

2013-04-10 | GSE45928 | GEO

Gene expression profiling of Capan-1 and Pt45P1 cells treated or not with alternatively spliced tissue factor (asTF)

Project description:The effects of alternatively spliced tissue factor (asTF) were measured by gene expression profiling of Capan-1 and Pt45P1 cells. 4 samples: Capan-1 cells +/- asTF, Pt45P1 cells +/- asTF.

2013-04-10 | E-GEOD-45928 | biostudies-arrayexpress

Validation of alternatively spliced protein isoforms in human mesenchymal stem cells

Project description:Alternative splicing of mRNA diversifies the function of human proteins, with tissue- and cell-specific protein isoforms being the most difficult to validate. While transcriptomic experiments enable the detection of many alternatively spliced transcripts, it is not known if these transcripts have protein-coding potential. We recently published the PG Nexus pipeline, which facilitates high confidence validation of exons and exon-exon junctions of spliced transcripts by integrating transcriptomics and proteomics data. Using the PG Nexus, we analyzed undifferentiated human mesenchymal stem cells and compared the number of protein isoforms validated using different protein sequence database, including public online databases and RNA-seq derived databases. With significant overlaps with other databases, we identified 8,011 exons and 3,824 splice junctions with the Ensembl database. Both exonic and junction peptides were important for protein isoform validation. The Ensembl database consistently outperformed the other data sources, but predicted open reading frames from RNA-seq derived transcripts were comparable, with only 6 less splice junctions validated. Using proteotypic and isoform-specific peptides, we validated 462 protein isoforms. This number increases to 1,083 if multiple proteotypic peptides per protein are included. Multiplexing proteotypic peptides in SRM assays or similar experiments will increase the confidence and coverage of protein isoform validation experiments.

2015-05-20 | PXD001449 | Pride

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