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PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

ABSTRACT: PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

PROVIDER: PRJNA778646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16848314_1.fastq.gz	Fastqsanger.gz
	SRR16848314_2.fastq.gz	Fastqsanger.gz
	SRR16848315_1.fastq.gz	Fastqsanger.gz
	SRR16848315_2.fastq.gz	Fastqsanger.gz
	SRR16848316_1.fastq.gz	Fastqsanger.gz

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PPIB-regulated alternative splicing of cell cycle genes contributes to the regulation of cell proliferation.

Project description:BackgroundPeptidylprolyl cis-trans isomerase B (PPIB) plays an important role in the process of inflammation through binding RNA, but the molecular pathogenesis is not yet clearly understood. The objective of this study was to investigate and verify the PPIB-regulated gene expressions and alternative splicing in Hela cells.MethodsWe examined the PPIB-regulated transcriptomes in HeLa cells using RNA-seq data. Differentially expressed genes, alternative splicing analysis were carried out. Functional enrichment analysis was used to define the enrichment of each term.ResultsWe found that PPIB knockdown successfully downregulated PPIB in Hela cells, which promoted cell proliferation (P < 0.001), but no significant effect on cell apoptosis. Ten alternative splicing genes regulated by PPIB were detected in Hela cells. The ten top Gene Ontology biological process analysis and functional pathways of the alternative splicing genes were screened and identified. The pathways where differentially expressed genes are most enriched were toll-like receptor 4 signaling pathways and other signaling pathways relating to inflammation and immune response. In addition, PPIB affects the alternative splicing of multiple genes, and the Gene Ontology-biological process analysis showed that genes significantly related to alternative splicing changes were mainly enriched in the cell cycle (P < 0.05).ConclusionPPIB regulates the alternative splicing of cell cycle-related genes to affect cell proliferation and regulate the occurrence and development of chronic inflammatory diseases such as Nasal polyps.

| S-EPMC9556483 | biostudies-literature

PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

Project description:Background: Peptidylprolyl cis-trans isomerase B (PPIB) plays an important function in the process of inflammation through binding RNA, but the clear molecular pathogenesis is not completely understood. The objective of this study was to investigate the PPIB-regulated gene expression and alternative splicing.

2022-10-28 | GSE188372 | GEO

Alternative Splicing of Pericentrin Contributes to Cell Cycle Control in Cardiomyocytes.

Project description:Induction of cardiomyocyte proliferation is a promising option to regenerate the heart. Thus, it is important to elucidate mechanisms that contribute to the cell cycle arrest of mammalian cardiomyocytes. Here, we assessed the contribution of the pericentrin (Pcnt) S isoform to cell cycle arrest in postnatal cardiomyocytes. Immunofluorescence staining of Pcnt isoforms combined with SiRNA-mediated depletion indicates that Pcnt S preferentially localizes to the nuclear envelope, while the Pcnt B isoform is enriched at centrosomes. This is further supported by the localization of ectopically expressed FLAG-tagged Pcnt S and Pcnt B in postnatal cardiomyocytes. Analysis of centriole configuration upon Pcnt depletion revealed that Pcnt B but not Pcnt S is required for centriole cohesion. Importantly, ectopic expression of Pcnt S induced centriole splitting in a heterologous system, ARPE-19 cells, and was sufficient to impair DNA synthesis in C2C12 myoblasts. Moreover, Pcnt S depletion enhanced serum-induced cell cycle re-entry in postnatal cardiomyocytes. Analysis of mitosis, binucleation rate, and cell number suggests that Pcnt S depletion enhances serum-induced progression of postnatal cardiomyocytes through the cell cycle resulting in cell division. Collectively, our data indicate that alternative splicing of Pcnt contributes to the establishment of cardiomyocyte cell cycle arrest shortly after birth.

| S-EPMC8397033 | biostudies-literature

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

2022-05-11 | GSE191022 | GEO

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

2022-05-11 | GSE191023 | GEO

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

| PRJNA789474 | ENA

Alternative splicing regulation of cell-cycle genes by SPF45/SR140/CHERP complex controls cell proliferation.

Project description:The regulation of pre-mRNA processing has important consequences for cell division and the control of cancer cell proliferation, but the underlying molecular mechanisms remain poorly understood. We report that three splicing factors, SPF45, SR140, and CHERP, form a tight physical and functionally coherent complex that regulates a variety of alternative splicing events, frequently by repressing short exons flanked by suboptimal 3' splice sites. These comprise alternative exons embedded in genes with important functions in cell-cycle progression, including the G2/M key regulator FOXM1 and the spindle regulator SPDL1. Knockdown of either of the three factors leads to G2/M arrest and to enhanced apoptosis in HeLa cells. Promoting the changes in FOXM1 or SPDL1 splicing induced by SPF45/SR140/CHERP knockdown partially recapitulates the effects on cell growth, arguing that the complex orchestrates a program of alternative splicing necessary for efficient cell proliferation.

| S-EPMC8594467 | biostudies-literature

PRPF6 regulated alternative splicing in colon cancer cell lines

Project description:PRPF6, an RNA binding component of the pre-mRNA spliceosome, is an essential driver of oncogenesis in colon cancer. PRPF6 is both amplified and overexpressed in colon cancer and cells with high PRPF6 levels are sensitive to its loss. Here we investigate alternative splicing changes in colon cancer cell lines following PRPF6 silencing by three different siRNA sequences. Two colon cancer cell lines (SW620 and KM-12), silencing of PRPF6 and control, 3 biological replicate samples for each group.

2014-06-18 | E-GEOD-56846 | biostudies-arrayexpress

Alternative splicing regulation of cell cycle genes by SPF45/SR140/CHERP complex controls cancer cell proliferation

Project description:Alternative splicing regulation of cell cycle genes by SPF45/SR140/CHERP complex controls cancer cell proliferation

| PRJNA749954 | ENA

Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

Project description:RBM5, a regulator of alternative splicing of apoptotic genes, and its close homologues, RBM6 and RBM10, are RNA binding proteins frequently deleted or mutated in lung cancer. We report that RBM5/6 and RBM10 antagonistically regulate the proliferative capacity of cancer cells and display distinct positional effects in alternative splicing regulation. We identify the Notch pathway regulator NUMB as a key target of these factors in the control of cell proliferation. NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation and its modulation recapitulates or antagonizes the effects of RBM5, 6 and 10 in cell colony formation. RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth. Our results reveal a key genetic circuit in the control of cancer cell proliferation. RNA from 3 biological replicates of knockdowns of RBM5, 6 and 10 and a control set were used. Changes between the control and knockdowns were measured based on using a splice-junction array (Affymetrix HJAY).

2013-12-20 | E-GEOD-47431 | biostudies-arrayexpress

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