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Analysis of gene expression and splicing after doxycycline-induced knockdown of SRSF3

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71745 | GEO | 2015/08/06

SECONDARY ACCESSION(S): PRJNA291985

REPOSITORIES: GEO

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Analysis of gene expression and splicing after doxycycline-induced knockdown of SRSF3

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

SRSF3-mediated regulation of N6-methyladenosine modification-related lncRNA ANRIL splicing in promotion of pancreatic cancer resistance to gemcitabine II

Project description:Serine/arginine-rich splicing factor 3 (SRSF3) functions to regulate mRNA alternative splicing, a molecular mechanism to process more than 90% of the protein-coding genes and provides an essential source for the biological versatility and targeting of SRSF3 could be a novel approach for cancer therapy. This study identify that SRSF3 expression was upregulated in pancreatic cancer tissues and associated with drug resistance and poor prognosis. Thus, we found that SRSF3 regulated ANRIL splicing and modified m6A modification of ANRIL in pancreatic cancer cells. More importantly, we demonstrated that the m6A methylation on lncRNA-ANRIL was essential for splicing process. Meanwhile, we also found that the different isoforms of ANRIL were differentially expressed in drug-resistant pancreatic cancer cell lines, and SRSF3 promotes gemcitabine resistance by regulating the expression of ANRIL-208. In addition, ANRIL-208 regulated pancreatic cancer cell chemoresistance by forming a complex with Ring1b and EZH2 and enhanced DNA homologous recombination repair (HR) capacity. In conclusion, the current study first established the link among SRSF3, m6A modification, lncRNA splicing, and DNA HR repair in pancreatic cancer, and first demonstrated that abnormal alternative splicing and m6A modification are closely related to chemotherapy resistance in pancreatic cancer.

2022-05-11 | GSE197532 | GEO

SRSF3-mediated regulation of N6-methyladenosine modification-related lncRNA ANRIL splicing in promotion of pancreatic cancer resistance to gemcitabine I

2022-05-11 | GSE197352 | GEO

The differentially expressed genes in SRSF3 siRNA-treated HCT116 cells

2013-08-04 | GSE31876 | GEO

The differentially expressed genes in SRSF3 siRNA-treated HCT116 cells

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

RNA-Seq analysis of SRSF3 KO hearts compared to controls and iCLIP analysis of SRSF3 binding profile in neonatal cardiomyocytes

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

Cardiomyocyte-specific Srsf3 deletion reveals a mitochondrial regulatory role

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

Transcriptome-wide analysis of wild-type and SRSF3-knockout glioma stem-like cells

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

Transcriptome analysis on TDP43 and SRSF3 downstream genes and binding RNAs in MDA-MB231 cells by Next Generation Sequencing

Project description:TDP43 and SRSF3 has been reported to be RNA-binding proteins; however their roles in breast cancer progression has not been examined previously. Here, we performed RNA-seq on MDA-MB231 cells stably expressed sh-control, shTDP43, shSRSF3 or sh-TDP43 and sh-SRSF3 using lentivirus in duplicates. In addition, MDA-MB231 cells with stable expression of flag-TDP43 or flag-SRSF3 were also generated by using lentivirus. RIP-seq was also applied to identify binding RNA against Flag antibodies.

2018-12-31 | GSE98016 | GEO

irCLIP of SRSF3 in a mouse epicardial cell line

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