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DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [tissues]

ABSTRACT: Alternative splicing (AS) events have been considered one of the critical hallmarks of cancer progression. However, the significance of ASE in HCC metastasis is not fully revealed. This study aims to investiage the important role of differential splicing events in HCC metastasis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183250 | GEO | 2024/08/31

REPOSITORIES: GEO

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DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [Cells]

Project description:The mechanism underlying hepatocellular carcinoma (HCC) metastasis remains unclear, many oncogenes are known to regulate this process. However, the role of alternative splicing (AS) in pro-metastatic HCC is poorly understood. The current study aimed to explore the function and molecular mechanism of DDX17 in alternative splicing.

2024-08-24 | GSE182787 | GEO

DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [tissues]

Project description:DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [tissues]

| PRJNA759786 | ENA

DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [Cells]

Project description:DDX17-regulated alternative splicing that produced a novel oncogenic isoform of PXN-AS1 to promote HCC metastasis [Cells]

| PRJNA757778 | ENA

DDX17-regulated alternative splicing that produced an oncogenic isoform of PXN-AS1 to promote HCC metastasis.

Project description:Background and aimsThe mechanism underlying HCC metastasis remains unclear, many oncogenes are known to regulate this process. However, the role of alternative splicing (AS) in pro-metastatic HCC is poorly understood.Approach and resultsBy performing RNA sequencing on nine pairs of primary HCC tissues with extrahepatic metastasis (EHMH) and nine pairs of metastasis-free HCC (MFH) tissues, we depicted the AS landscape in HCC and found a higher frequency of AS events in EHMH compared with MFH. Moreover, 28 differentially expressed splicing regulators were identified in EHMH compared with MFH. Among these, DEAD-box RNA helicase 17 (DDX17) was significantly up-regulated in EHMH and was strongly associated with patient outcome. Functional studies indicated that DDX17 knockout inhibited the degradation of the extracellular matrix, and diminished the invasive ability of HCC cells. A significant reduction in lung metastasis induced by DDX17 deficiency was also demonstrated in a diethylnitrosamine-induced DDX17HKO mouse model. Mechanistically, high DDX17 induced intron 3 retention of PXN-AS1 and produced a transcript (termed PXN-AS1-IR3). The transcript PXN-AS1-IR3 acted as an important promoter of HCC metastasis by inducing MYC transcription activation via recruiting the complex of testis expressed 10 and p300 to the MYC enhancer region, which led to transcriptional activation of several metastasis-associated downstream genes. Finally, the PXN-AS1-IR3 level was significantly higher in serum and HCC tissues with extrahepatic metastasis.ConclusionsDDX17 and PXN-AS1-IR3 act as important metastatic promoters by modulating MYC signaling, suggesting that DDX17 and PXN-AS1-IR3 may be potential prognostic markers for metastatic HCC.

| S-EPMC9304246 | biostudies-literature

Identification of allele-specific alternative mRNA processing via transcriptome sequencing

Project description:Establishing the functional roles of genetic variants remains a significant challenge in the post-genomic era. Here, we present a method, allele-specific alternative mRNA processing (ASARP), to identify genetically influenced mRNA processing events using transcriptome sequencing (RNA-Seq) data. The method examines RNA-Seq data at both single nucleotide and whole-gene/isoform levels to identify allele-specific expression (ASE) and existence of allele-specific regulation of mRNA processing. We applied the methods to data obtained from the human glioblastoma cell line U87MG and primary breast cancer tissues and found that 26M-bM-^@M-^S45% of all genes with sufficient read coverage demonstrated ASE, with significant overlap between the two cell types. Our methods predicted potential mechanisms underlying ASE due to regulations affecting either whole-gene-level expression or alternative mRNA processing, including alternative splicing, alternative polyadenylation and alternative transcriptional initiation. Allele-specific alternative splicing and alternative polyadenylation may explain ASE in hundreds of genes in each cell type. Reporter studies following these predictions identified the causal single nucleotide variants (SNVs) for several allele-specific alternative splicing events. Finally, many genes identified in our study were also reported as disease/phenotype-associated genes in genome-wide association studies. Future applications of our approach may provide ample insights for a better understanding of the genetic basis of gene regulation underlying phenotypic diversity and disease mechanisms. Examine allele-specific gene expression and alternative RNA processing in U87MG cell line

2012-03-29 | E-GEOD-29738 | biostudies-arrayexpress

A Novel Functional Splice Variant of AKT3 Defined by Analysis of Alternative Splice Expression in HPV-Positive Oropharyngeal Cancers (MBD-Seq)

Project description:The incidence of HPV-related oropharyngeal squamous cell carcinoma (OPSCC) has increased more than 200% in the past 20 years. Recent genetic sequencing efforts have elucidated relevant genes in head and neck cancer, but HPV-related tumors have consistently shown few DNA mutations. In this study, we sought to analyze alternative splicing events (ASE) that could alter gene function independent of mutations. To identify ASE unique to HPV-related tumors, RNA sequencing was performed on 46 HPV-positive OPSCC and 25 normal tissue samples. A novel algorithm using outlier statistics on RNA-sequencing junction expression identified 109 splicing events, which were confirmed in a validation set from The Cancer Genome Atlas.

2018-03-20 | GSE112023 | GEO

A Novel Functional Splice Variant of AKT3 Defined by Analysis of Alternative Splice Expression in HPV-Positive Oropharyngeal Cancers (RNA-Seq)

2018-03-20 | GSE112026 | GEO

Identification of allele-specific alternative mRNA processing via transcriptome sequencing

Project description:Establishing the functional roles of genetic variants remains a significant challenge in the post-genomic era. Here, we present a method, allele-specific alternative mRNA processing (ASARP), to identify genetically influenced mRNA processing events using transcriptome sequencing (RNA-Seq) data. The method examines RNA-Seq data at both single nucleotide and whole-gene/isoform levels to identify allele-specific expression (ASE) and existence of allele-specific regulation of mRNA processing. We applied the methods to data obtained from the human glioblastoma cell line U87MG and primary breast cancer tissues and found that 26–45% of all genes with sufficient read coverage demonstrated ASE, with significant overlap between the two cell types. Our methods predicted potential mechanisms underlying ASE due to regulations affecting either whole-gene-level expression or alternative mRNA processing, including alternative splicing, alternative polyadenylation and alternative transcriptional initiation. Allele-specific alternative splicing and alternative polyadenylation may explain ASE in hundreds of genes in each cell type. Reporter studies following these predictions identified the causal single nucleotide variants (SNVs) for several allele-specific alternative splicing events. Finally, many genes identified in our study were also reported as disease/phenotype-associated genes in genome-wide association studies. Future applications of our approach may provide ample insights for a better understanding of the genetic basis of gene regulation underlying phenotypic diversity and disease mechanisms.

2012-03-30 | GSE29738 | GEO

DIS3 dysfunction suppresses altered alternative splicing in cells with the depletion of U2 snRNP component

Project description:Precise analysis of DIS3 interactors disclosed in genome-wide siRNA screening revealed enrichment in genes responsible for transcription and processes highly connected to it like splicing and 3’ end formation. Among the strongest positive interactors were components of of SF3a complex and some of SF3b complex. SF3a complex is a substantial integral component of the pre-spliceosome and is required for complex A and B assembly and plays crucial role in initial steps of spliceosome assembly.Transcriptome analysis demonstrated that depletion of SF3A1, one of three SF3a complex components, lead to extensive alterations in multiple classes of alternative splicing events (ASE). Remarkably, the only group of ASE that was reshaped in the presence of DIS3 dysfunction was intron retention. Detailed investigations of transcripts with altered intron retention revealed high enrichment in transcripts coding ribosomal proteins (Rps).

2021-03-31 | GSE155123 | GEO

RNA-Binding Protein Trx regulates alternative splicing and promotes metastasis of HCC via interacting with LINC00152

Project description:RNA-binding proteins (RBPs) were reported to be the key regulator of epithelial-mesenchymal transition (EMT)-related post-transcriptional in tumor diseases.To explore the role of RBPs in metastasis of hepatocellular To explore the role of RBPs in metastasis of hepatocellular carcinoma (HCC), whole transcription sequencing was conducted to identify differential RBPs between HCC with metastasis or without metastasis. The influence of RBPs on metastasis of HCC was verified by in vitro and in vivo experiments. Interaction of RBPs with non-coding RNAs was evaluated by RNA immune-precipitation and pull-down assay. RNA-seq whole genome sequencing and alternative splicing analysis were further performed to clarify post-transcription regulation mechanisms.

2023-10-24 | GSE245587 | GEO

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