Transcriptome-wide analysis of wild-type and SRSF3-knockout glioma stem-like cells
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PROVIDER: PRJNA540487 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The splicing factor SRSF3 is a member of serine- and arginine-rich proteins, which is frequently upregulated in various types of cancer. The aim of this study is to profile the alternative splicing (AS) events that were regulated by SRSF3 in glioma stem-like cells (GSCs). Methods: Total RNAs isolated from GSC83 and GSC528 cells with SRSF3-konckout (KO) or control (WT) were subjected to paired-end RNA-seq using the Illumina NextSeq 500 system according to the manufacturer's instruction. Raw reads were subjected to quality control and then aligned with HISAT2 to the human genome hg19. Quantification was performed using HTSeq-count. Differential expression of genes was calculated by DESeq2. For the splicing analysis, the mapped reads were processed through the MISO pipeline to estimate expression of alternatively spliced isoforms. The PSI (Percent Spliced In) values were calculated for each annotated AS event. Results: We identified a total of 2752 and 2548 SRSF3-regulated AS events in GSC83 and 528 cells, respectively, with 1143 events shared by these two GSC cell lines. Conclusions: Our study defines SRSF3 as a master regulator of glioma-associated AS program, implicating SRSF3 as an oncogenic factor for tumorigenesis and a potential therapeutic target for GBM treatment.
2019-09-21 | GSE130501 | GEO
Project description:Serine-rich splicing factor 3 (SRSF3) was recently reported as being necessary to preserve RNA stability via an mTOR mechanism in a cardiac mouse model in adulthood. Here, we demonstrate the link between Srsf3 and mitochondrial integrity in an embryonic cardiomyocyte-specific Srsf3 conditional knockout (cKO) mouse model. Fifteen-day-old Srsf3 cKO mice showed dramatically reduced (below 50%) survival and reduced the left ventricular systolic performance, and histological analysis of these hearts revealed a significant increase in cardiomyocyte size, confirming the severe remodeling induced by Srsf3 deletion. RNA-seq analysis of the hearts of 5-day-old Srsf3 cKO mice revealed early changes in expression levels and alternative splicing of several transcripts related to mitochondrial integrity and oxidative phosphorylation. Likewise, the levels of several protein complexes of the electron transport chain decreased, and mitochondrial complex I-driven respiration of permeabilized cardiac muscle fibers from the left ventricle was impaired. Furthermore, transmission electron microscopy analysis showed disordered mitochondrial length and cristae structure. Together with its indispensable role in the physiological maintenance of mouse hearts, these results highlight the previously unrecognized function of Srsf3 in regulating the mitochondrial integrity.
2021-06-23 | GSE151168 | GEO
Project description:Human glioma stem cell GS5: Control vs. ZNF117 knockout
| PRJNA777547 | ENA
Project description:Several members of SRSF family play wide-ranging roles in the regulation of transcription and post-splicing processes as well as splice sites selection. Although the expression of SRSF3 was reported to be overexpressed in several cancers, the roles of SRSF3 in the cancer cells are almost unknown. We analyzed differentially expressed genes in SRSF3 siRNA-treated HCT116 cells and identified the specific pathways regulated by SRSF3. After treatment of HCT116 cells with SRSF3 (sample 02) or control (sample 01) siRNA, total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA). The quality of the purified RNA and its applicability for microarray analysis were assessed by the Agilent 2100 Bioanalyzer using a RNA 6000 Nano Labchip kit (Agilent Technologies, Palo Alto, CA, USA). Total RNA (400 ng) was used for amplification, labeling and hybridization to a whole human genome oligoDNA microarray (4x44k; Agilent) according to the manufacture’s instructions.
2013-08-04 | E-GEOD-31876 | biostudies-arrayexpress
Project description:The goal of this study is to analyse the transcriptome of control hearts vs hearts lacking SRSF3 expression and to analyse binding preferences of SRSF3 in cardiac myocytes.
2019-05-27 | GSE123002 | GEO
Project description:Several members of SRSF family play wide-ranging roles in the regulation of transcription and post-splicing processes as well as splice sites selection. Although the expression of SRSF3 was reported to be overexpressed in several cancers, the roles of SRSF3 in the cancer cells are almost unknown. We analyzed differentially expressed genes in SRSF3 siRNA-treated HCT116 cells and identified the specific pathways regulated by SRSF3.
2013-08-04 | GSE31876 | GEO
Project description:SRSF3 is overexpressed in human invasive ovarian cancer and its overexpression is required for cancer cell growth and survival. To decipher the mechnisms behind the role of SRSF3 in ovarian cancer, we examined the gene expression and splicing in the ovarian cancer cell line that was engineered to express a doxycycline-induced SRSF3 siRNA, which was able to knockdown SRSF3 expression by 90% and induce apoptosis. Total RNAs extracted from A2780/SRSF3si2, a subline of ovarian cancer cell line A2780, treated with or without doxycycline at 0.1ug/ml for three days were analyzed using Affymetrix GeneChip® Human Exon 1.0 ST Array
2015-08-06 | E-GEOD-71745 | biostudies-arrayexpress
Project description:SRSF3 is overexpressed in human invasive ovarian cancer and its overexpression is required for cancer cell growth and survival. To decipher the mechnisms behind the role of SRSF3 in ovarian cancer, we examined the gene expression and splicing in the ovarian cancer cell line that was engineered to express a doxycycline-induced SRSF3 siRNA, which was able to knockdown SRSF3 expression by 90% and induce apoptosis.
2015-08-06 | GSE71745 | GEO
Project description:This experiment aims to map SRSF3 binding to the global transcriptome in a mouse epicardial cell line
2022-12-31 | E-MTAB-11853 | biostudies-arrayexpress
Project description:Understanding the glioma stem cell (GSC) heterogeneity within IDH1 and TP53 mutant tumors may elucidate possible targets for astrocytoma treatment. We performed single-nucleus transcriptomics of 6 mutant and wild-type glioma samples sorted for Sox2 stem cell marker. Malignant states of different clusters were evaluated by the expression of the normal and hematopoietic markers. We found that mutant GSCs were characterized by collagen synthesis and CD44-high phenotype prone to migration, while wild-type GSCs had vulnerability points in ATP synthesis. Additionally, mutant GSCs displayed altered lipogenesis probably attributed to the low NADPH consumed by mutant IDH1. The collagen and lipid biosynthesis represent possible target pathways for prospective tackling GSCs with IDH1 R132H and TP53 point mutations, uncouplers of oxidative phosphorylation are promising to address wild-type GSC proliferation
2021-01-12 | GSE164624 | GEO