RBM4 modulate apoptosis and expression of inflammatory factors via alternative splicing in HeLa cells
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ABSTRACT:
PROVIDER: PRJNA555059 | ENA |
REPOSITORIES: ENA
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Project description:We overexpressed RBM4 in HeLa cells to study RBM4-regulated genes using RNA-seq technology, followed by bioinformatic analysis of target genes of RBM4-regulated transcriptional factors (TFs)
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Project description:RBM4 is a RNA-binding protein (RBP) able to modulate splicing by promoting exon inclusion and shares an import pathway with other splicing factors in the nucleus. In earlier studies we found that RBM4 interacts and colocalizes with WT1, which has been implicated in 10M-bM-^@M-^S15% of WilmsM-bM-^@M-^Y tumours and more recently in leukemya, is considered to be a tumour suppressor. RBM4, a RBP whose splicing effect is inhibited by the +KTS isoform of the tumour-suppressor/activator WT1, exhibits altered expression in different tumours, and may be essential for proliferation. Moreover, RBM4 binds to a number of RNAs of genes involved in acute myeloid leukaemia and cell cycle control. These results suggest that RBM4 may be involved in alternative splicing, tumorigenesis and particularly leukaemogenesis. To determine the endogenous transcripts that are targeted by RBM4 at the genome-wide level, we decided to perform exon microarray studies. RBM4-specific siRNA has been used for knockdown of RBM4 in HeLa cells. RNA was extracted using a Qiagen RNA extraction kit from untransfected, mock and siRNA-transfected HeLa cells and quality of RNA for microarray analysis was checked using a Bioanalyzer 2100 (Agilent Technologies). Experiments were run in triplicates.
2012-07-14 | E-GEOD-32933 | biostudies-arrayexpress
Project description:RBM4 is a RNA-binding protein (RBP) able to modulate splicing by promoting exon inclusion and shares an import pathway with other splicing factors in the nucleus. In earlier studies we found that RBM4 interacts and colocalizes with WT1, which has been implicated in 10–15% of Wilms’ tumours and more recently in leukemya, is considered to be a tumour suppressor. RBM4, a RBP whose splicing effect is inhibited by the +KTS isoform of the tumour-suppressor/activator WT1, exhibits altered expression in different tumours, and may be essential for proliferation. Moreover, RBM4 binds to a number of RNAs of genes involved in acute myeloid leukaemia and cell cycle control. These results suggest that RBM4 may be involved in alternative splicing, tumorigenesis and particularly leukaemogenesis. To determine the endogenous transcripts that are targeted by RBM4 at the genome-wide level, we decided to perform exon microarray studies.
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Project description:Gene expression and splicing switches upon RBM4 overexpression 2 Samples
2014-09-18 | E-GEOD-58594 | biostudies-arrayexpress
Project description:Gene expression and splicing switches upon RBM4 overexpression
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Project description:RNA-seq was performed on A549 and H1299 cells that stably knocking down RBM4 or control, in order to profile the gene expression change that were regulated by RBM4
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Project description:Cytokeratin 18(CK18), one of the major components of intermediate filaments (IF) in simple-type epithelial cells, has been used as the biomarker of several cancers. CK18 has been also reported to be dysregulated in cervical cancers, however, the precise molecular pathways regulated by CK18 remained elusive. In this study, CK18 was knockdown in Hela cells and which led to a significantly decrease of cell apoptosis compared with control cells. The global transcript profile and alternative splicing of CK18 knockdown cells and control were analyzed. A total of 593 differentially expressed genes were identified, and these genes were mainly involved in synaptic transmission, immune response, innate immune response, signal transduction pathways. Strikingly, hundreds of genes were regulated by CK18, which mainly enriched in immune and apoptosis related pathways. In conclusion, our study indicates that CK18 plays important regulatory role in cervical cancers in transcriptional level as well as alternative splicing regulation.
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Project description:RNA binding proteins have important functions in tumorigenesis; therefore, their regulatory mechanisms should be further explored. The present study aimed to determine the regulatory roles of RNA binding motif protein 6 (RBM6) in transcription and alternative splicing in Hela cells. RBM6 expression levels and its effect on the prognosis of different tumors in The Cancer Genome Atlas database were analyzed using TIMER2.0. Short hairpin RNA was used to ablate RBM6 expression in HeLa cells. Differentially expressed genes and alternative splicing events in Hela cells were assessed using RNA sequencing and quantitative real-time reverse transcription polymerase chain reaction. RBM6 was identified as a prognostic marker for bladder urothelial carcinoma, kidney renal clear cell carcinoma, mesothelioma, and pancreatic adenocarcinoma. Knockdown of RBM6 promoted cell proliferation. In Hela cells, RMB6 regulated the expression and alternative splicing of many genes involved in tumorigenesis_x001E_related pathways, including ‘apoptotic process’, ‘mitotic cell cycle’, and ‘RNA splicing’. RBM6-regulated alternatively spliced genes (DIABLO (Diablo IAP-binding mitochondrial protein), PAK4 (P21 (RAC1) activated kinase 4) and ERCC2 (ERCC excision repair 2, TFIIH core complex helicase subunit)) were subjected to quantitative real-time reverse transcription polymerase chain reaction validation, which demonstrated the same expression trends as the RNA sequencing results. Our findings showed that RBM6 affects tumorigenesis and cancer progression by disrupting alternative splicing in HeLa cells.
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Project description:Post-transcriptional mechanisms is an important means for the body to fight against cancer, and it may also be hijacked by tumor cells to help them adapt to local microenvironment. Filamin B (FLNB), an actin-binding protein and providing crucial scaffolds for cell motility and signaling, was also identified as one of RNA binding proteins (RBPs). Recent works showed that FLNB might play important role not only in skeletal development but also in the regulation of tumorigenesis. However, the effects of dysregulated expression of FLNB at a molecular level are unclear. In this study, we used RNA-seq to analyze the global transcriptional level changes and alternative splicing between the knocked-down FLNB and the control in Hela cells. Reduced levels of FLNB led to a significant decrease in cell apoptosis, compared with control cells. FLNB knockdown extensively regulated the expression of genes in cell apoptosis, tumorigenesis, metastases, transmembrane transport, cartilage and nerve development. Moreover, FLNB regulated alternative splicing of a large number of genes enriched in cell death and apoptotic process. Meanwhile, some genes and alternative splicing related to skeletal development were enriched and regulated by FLNB. Quantitative RT-PCR confirmed the FLNB-regulated transcription and alternative splicing. This study provides the first transcriptome-wide analysis of FLNB. Our findings indicated that FLNB may play an important regulatory role in cancer cell apoptosis via the regulation of alternative splicing and potentially transcription, which greatly expands the current understanding of the mechanisms of FLNB mediated gene regulation.
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Project description:To identify which mRNAs bind to RBM4/HIF-2a Two PAR-CLIPs were performed: One of an RBM4 immunoprecipitation, and the other of a HIF-2a immunoprecipitation and excising the associated RBM4 band.
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