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RBM39 promotes hepatocarcinogenesis by regulating RFX1's alternative splicing and subsequent activation of integrin signaling pathway

ABSTRACT: RBM39 promotes hepatocarcinogenesis by regulating RFX1's alternative splicing and subsequent activation of integrin signaling pathway

PROVIDER: PRJNA1150507 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30327501_1.fastq.gz	Fastqsanger.gz
	SRR30327501_2.fastq.gz	Fastqsanger.gz
	SRR30327502_1.fastq.gz	Fastqsanger.gz
	SRR30327502_2.fastq.gz	Fastqsanger.gz
	SRR30327503_1.fastq.gz	Fastqsanger.gz

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RBM39 promotes hepatocarcinogenesis by regulating RFX1's alternative splicing and subsequent activation of integrin signaling pathway

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 | GSE275347 | GEO

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

2025-03-03 | GSE275496 | GEO

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

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

| PRJNA1151090 | ENA

ChIP-seq for RFX1

Project description:ChIP-seq for RFX1

| PRJNA866861 | ENA

RNA-seq Analysis of RFX1-dependent Genes in Fusarium graminearum Z-3639

Project description:Fusarium graminearum is a major pathogen of Fusarium head blight in wheat, barley, and rice, as well as ear rot and stalk rot in maize. Regulatory Factor X (RFX) transcription factors are well-conserved in animals and fungi, but their functions are diverse, ranging from DNA-damage response to ciliary gene regulation. We investigated the role of the sole RFX transcription factor, RFX1, in F. graminearum. Deletion of rfx1 resulted in multiple defects in hyphal growth, conidiation, virulence, and sexual development. Deletion mutants of rfx1 were more sensitive to various types of DNA damage than the wild-type strain. Septum formation was inhibited and micronuclei were produced in the rfx1 deletion mutants. The results of the neutral comet assay demonstrated that disruption of rfx1 function caused spontaneous DNA double-strand breaks. To understand regulatory mechanisms of rfx1 in F. graminearum, we obtained and analyzed genome-wide transcription profiles generated from the RNA-sequencing data of the wild-type and M-NM-^Trfx1 strains. RNA-sequencing-based transcriptomic analysis revealed that RFX1 suppressed the expression of many genes, including genes for the repair of DNA damage. 2 samples examined: mycelia harvested 24 h after inoculation of wild-type conidia in complete medium; mycelia harvested 32 h after inoculation of M-NM-^Trfx1 conidia in complete medium

2014-01-28 | E-GEOD-52198 | biostudies-arrayexpress

RNA-seq Analysis of RFX1-dependent Genes in Fusarium graminearum Z-3639

Project description:Fusarium graminearum is a major pathogen of Fusarium head blight in wheat, barley, and rice, as well as ear rot and stalk rot in maize. Regulatory Factor X (RFX) transcription factors are well-conserved in animals and fungi, but their functions are diverse, ranging from DNA-damage response to ciliary gene regulation. We investigated the role of the sole RFX transcription factor, RFX1, in F. graminearum. Deletion of rfx1 resulted in multiple defects in hyphal growth, conidiation, virulence, and sexual development. Deletion mutants of rfx1 were more sensitive to various types of DNA damage than the wild-type strain. Septum formation was inhibited and micronuclei were produced in the rfx1 deletion mutants. The results of the neutral comet assay demonstrated that disruption of rfx1 function caused spontaneous DNA double-strand breaks. To understand regulatory mechanisms of rfx1 in F. graminearum, we obtained and analyzed genome-wide transcription profiles generated from the RNA-sequencing data of the wild-type and Δrfx1 strains. RNA-sequencing-based transcriptomic analysis revealed that RFX1 suppressed the expression of many genes, including genes for the repair of DNA damage.

2014-01-28 | GSE52198 | GEO

Study of RFX1 and RFX3 binding sites in the mouse genome

Project description:The aim of the study was to identify RFX1 and RFX2 binding sites in mouse pancreatic beta cells. Chromatin immunoprecipitation experiments were performed with the mouse MIN6 beta cell line and antibodies raised against RFX1 and RFX3. Immunoprecipitated DNA was sequenced using the Genome Analyzer II (Illumina). Antibodies were described in Reith W, Ucla C, Barras E, Gaud A, Durand B, Herrero-Sanchez C, Kobr M, Mach B : RFX1, a transactivator of hepatitis B virus enhancer I, belongs to a novel family of homodimeric and heterodimeric DNA-binding proteins. Mol Cell Biol 1994;14:1230–1244

2015-08-22 | E-GEOD-72272 | biostudies-arrayexpress

Effect of of RFX1 on regene expression in mouse peritoneal macrophages

Project description:To investigate the function of RFX1 in the regulation of macrophage polarization, we overexpressed RFX1 in mouse peritoneal macrophages(PMAs) by lentivirus infections. We then performed gene expression profiling analysis using data obtained from RNA-seq.

2024-08-06 | GSE236155 | GEO

Effect of RFX1 on gene expression and the potential binding target genes in LPS-stimulated macrophages [RNA-seq]

Project description:To investigate the function of RFX1 in the regulation of macrophage polarization, we overexpressed RFX1 in mouse peritoneal macrophages(PMAs) or human CD14+ derived macrophage(hMDMs) by lentivirus infections or reduce RFX1 expression in PMAs from mice with Rfx1 deficiency(CKO) . We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2023-11-08 | GSE210667 | GEO

Study of RFX1 and RFX3 binding sites in the mouse genome

Project description:The aim of the study was to identify RFX1 and RFX2 binding sites in mouse pancreatic beta cells.

2015-08-22 | GSE72272 | GEO