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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

ABSTRACT: MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

PROVIDER: PRJNA1034067 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26617702_1.fastq.gz	Fastqsanger.gz
	SRR26617702_2.fastq.gz	Fastqsanger.gz
	SRR26617703_1.fastq.gz	Fastqsanger.gz
	SRR26617703_2.fastq.gz	Fastqsanger.gz

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

Project description:RNA immunoprecipitation sequencing (RIP-seq) for the detection of RBM39 protein-binding RNA in SW480 cells.

2024-08-02 | GSE246656 | GEO

MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer

Project description:MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shRBM39 mRNA-seq]

Project description:MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shRBM39 mRNA-seq]

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shMORC2 mRNA-seq]

Project description:MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shMORC2 mRNA-seq]

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shMORC2 mRNA-seq]

Project description:To investigate the role MORC2 plays in alternative splicing, we generated SW480 cell lines in which MORC2 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

2024-08-02 | GSE246909 | GEO

MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shRBM39 mRNA-seq]

Project description:To investigate the role RBM39 plays in alternative splicing, we generated SW480 cell lines in which RBM39 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

2024-08-02 | GSE246915 | GEO

RBM39 promotes hepatocarcinogenesis by regulating RFX1's alternative splicing and subsequent activation of integrin signaling pathway [RIP-seq]

Project description:There is increasing evidence that alternative splicing (AS) is crucial for tumor cells because it can produce various protein isoforms that may play different or even opposing roles in tumor growth and metastasis. Despite its significance, the role of AS and related splicing factors, particularly splicing-related messenger ribonucleoproteins (mRNPs), in hepatocarcinogenesis is poorly understood. High-throughput transcriptome sequencing of HCC patients revealed that the spliceosome pathway may play an important role in HCC development. Through the combined analysis of the three gene clusters consisting of differentially expressed genes (DEGs), genes encoding RNA-binding proteins (RBPs) and genes related to splicing-related mRNPs, the splicing factor RBM39 was identified, which was highly expressed in HCC tumor tissues with prognostic value. Functional studies showed that RBM39 silencing inhibited cell proliferation, migration and invasion via the integrin pathway. By performing RNA immunoprecipitation sequencing (RIP-seq), we found that RBM39 combined with RFX1 pre-mRNA and regulated alternative splicing of its exon 2. Mechanistically, the skipping of exon 2 in RFX1, influenced by high RBM39 expression in HCC cells, led to production of an N-terminal truncated RFX1, which lost the ability to transcriptionally repress oncogenic collagen genes. This process further activated the downstream FAK/PI3K/AKT signaling pathway. Furthermore, we further validated these findings in the hydrodynamic tail vein injection (HTVI) mouse model and human HCC tissues. Therefore, we hypothesized that high RBM39 expression enhances the malignant capabilities of HCC cells by regulating the alternative splicing of RFX1 and subsequently activating the FAK/PI3K/AKT signaling pathway.

2025-03-03 | GSE275496 | GEO

MORC2 phosphorylation fine tunes its DNA compaction activity

Project description:Variants in the poorly characterised oncoprotein, MORC2, a chromatin remodelling ATPase, lead to defects in epigenetic regulation and DNA damage response. MORC2 variants are associated with multiple cancers and neurological disorders1,2. The C-terminal domain (CTD) of MORC2 is often phosphorylated in DNA damage response and is known to induce cancer progression in in vivo and in vitro cancer models3-5. However, it remains unclear how MORC2 CTD and its phosphorylation impacts its chromatin remodelling activity. Here, we report a molecular characterisation of full-length, phosphorylated MORC2. We show that MORC2 preferentially binds open chromatin, has multiple DNA binding sites with varying affinities and acts as a DNA sliding clamp. We identified a phosphate interacting motif within the CTD that dictates ATP hydrolysis and cooperative DNA binding. The DNA binding impacts several structural domains within the N-terminal ATPase region. We provide the first visual proof that MORC2 induces chromatin remodelling through ATP hydrolysis-dependent DNA compaction, where the speed of compaction is affected by its phosphorylation state. Together, our results reveal that phosphorylation of MORC2 CTD modulates its chromatin remodelling and could be an attractive target for therapeutics.

2025-05-05 | PXD053383 | Pride

MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer

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

2024-08-02 | GSE246916 | GEO

ATAC-seq profiling of mutated MORC2 overexpression in MORC2-knocked-out HEK293T cells

Project description:We report an in vitro reconstitution of full-length MORC2, the most commonly mutated MORC member, linked to various cancers and neurological disorders. MORC2 possesses multiple DNA binding sites that undergo structural rearrangement upon DNA binding. MORC2 locks onto the DNA using its C-terminal domain (CTD) and acts as a sliding clamp. A conserved phosphate-interacting motif within the CTD was found to regulate ATP hydrolysis and cooperative DNA binding. Importantly, MORC2 mediates chromatin remodelling via ATP hydrolysis-dependent DNA compaction, regulated by the phosphorylation state of its CTD.

2025-05-05 | GSE283383 | GEO

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