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SRSF6 -regulated alternative splicing of genes involved in DNA repair is associated with prostate cancer progression

ABSTRACT: SRSF6 -regulated alternative splicing of genes involved in DNA repair is associated with prostate cancer progression

PROVIDER: PRJNA576647 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10251241_1.fastq.gz	Fastqsanger.gz
	SRR10251241_2.fastq.gz	Fastqsanger.gz
	SRR10251242_1.fastq.gz	Fastqsanger.gz
	SRR10251242_2.fastq.gz	Fastqsanger.gz
	SRR10251243_1.fastq.gz	Fastqsanger.gz

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SRSF6 -regulated alternative splicing of genes involved in DNA repair is associated with prostate cancer progression

Project description:Alternative splicing (AS) occurs in nearly all human genes and abnormal AS has a close connection with cancer. SRSF6, a canonical member of the serine/arginine-rich (SR) protein family, has been characterized as an important regulator of AS. However, the role of SRSF6 in regulating AS in prostate cancer remains unclear. In this study we analyzed SRSF6 expression levels in 550 prostate cancer tissue samples available in The Cancer Genome Atlas database and found that expression of SRSF6 was upregulated in all prostate cancer stages we examined. To investigate the biological consequences of SRSF6 overexpression, we constructed an SRSF6-overexpressing cell model and utilized RNA-seq to explore transcriptional changes. We also selected two groups of prostate cancer tumor samples in which SRSF6 was differentially expressed to analyze potential SRSF6-regulated AS. We hypothesized that overexpression of SRSF6 in cancer cells would induce large-scale changes in transcriptional expression levels and AS. We found that the pattern of SRSF6-regulated AS in cancer cells was similar to that observed in clinical samples and was enriched in pathways like DNA repair, double-strand break repair via homologous recombination and others. We also validated SRSF6-regulated AS events using RT-qPCR. Our findings highlighted how SRSF6 could regulate DNA repair-related pathways via regulation of AS to influence cancer progression in both cancer cells and prostate cancer tumor samples. These results greatly expand our current understanding of the mechanisms underlying SRSF6-mediated gene regulation and suggests the potential use of SRSF6 as a cancer therapeutic target.

2020-10-20 | GSE138636 | GEO

Overexpression of splicing factor SRSF6 in mouse skin

Project description:Many biological processes involve post-transcriptional regulation of gene expression by alternative pre-mRNA splicing. Here, we show that an alternative splicing factor SRSF6 affects tissue homeostasis of the skin. In this dataset, we study effects on gene expression and alternative splicing upon SRSF6 overexpression (+doxycycline) in mouse skin using inducible R26-rtTA+/-, ColA1-TREtight-SRSF6+/- transgenic mice 4 mixed-background strain samples (2 SRSF6-induced skin samples and 2 uninduced skin control samples)

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Overexpression of splicing factor SRSF6 in mouse skin

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DRAK2 aggravates nonalcoholic fatty liver disease progression through SRSF6-associated RNA alternative splicing

Project description:Drak2 Regulates RNA Alternative Splicing by Suppressing SRPK1-SRSF6 Signaling Pathway

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SRSF6 regulates alternative splicing of genes involved in DNA damage response and DNA repair in HeLa cells.

Project description:Alternative splicing (AS) occurs in nearly all human genes and abnormal AS has a close association with cancer. Serine and arginine‑rich splicing factor 6 (SRSF6), a canonical member of the serine/arginine‑rich protein family, has been characterized as an important regulator of AS. However, the role of SRSF6 in regulating AS in cancers has remained to be fully elucidated. In the present study, the median expression of SRSF6 in tumors was determined to be higher compared with that in matched normal tissues in 13 out of 16 cancer types from The Cancer Genome Atlas. To investigate the biological effects of SRSF6 overexpression, an SRSF6‑overexpression model of HeLa cells was constructed and it was revealed that SRSF6 overexpression resulted in significantly higher apoptosis and lower proliferation compared to control cells. Transcriptome analysis indicated that overexpression of SRSF6 in cancer cells induced large‑scale changes in transcriptional expression levels and AS. Two groups of cervical cancer tumor samples in which SRSF6 was differentially expressed were then selected to analyze potential SRSF6‑regulated AS. It was determined that the pattern of SRSF6‑regulated AS in clinical samples was similar to that in cancer cells and AS genes were enriched in DNA damage response (DDR) pathways, including DNA repair and double‑strand break repair via homologous recombination. Furthermore, AS events regulated by SRSF6 were validated using reverse transcription‑quantitative PCR. The present results highlighted that SRSF6 is able to trigger the activation of DDR pathways via regulation of AS to influence cancer progression. These results markedly expand the current understanding of the mechanisms underlying SRSF6‑mediated gene regulation and suggest the potential use of SRSF6 as a therapeutic target in cancer.

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Project description:Pleural fibrosis is defined as an excessive deposition of extracellular matrix that results in destruction of the normal pleural tissue architecture and compromised function. There is no effective medication for this disorder. Pleural mesothelial cells (PMCs/ Met-5A) play a key role in the process of pleural fibrosis. However, the detailed mechanisms are poorly understood. In our study, firstly SRSF6 protein has a major role in pleural fibrosis progression. To explore downstream of SRSF6, RNA sequencing was performed in Met-5A treated by bleomycin(0.2ug/ml) with SRSF6 siRNA or negtive control siRNA (siRNA NC). In conclusion, SRSF6 induced pleural fibrosis through a cluster pathway including SRSF6/WNT5A and SRSF6/SMAD1/5/9 signaling. SRSF6 is involved in pleural fibrosis, inhibition of SRSF6 is a novel strategy for treatment.

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Project description:The downregulation of diabetes susceptibility gene GLIS3 contributes to pancreatic beta cell demise, at least in part, through downregulation of the splicing factor SRSF6. Here, we used individual-nucleotide UV crosslinking and immunoprecipitation (iCLIP) to map the RNA binding landscape of SRSF6 in pancreatic beta cells.

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LncRNA CRNDE attenuates chemoresistance in gastric cancer via SRSF6-regulated alternative splicing of PICALM.

Project description:De novo and acquired resistance, which are mainly mediated by genetic alterations, are barriers to effective routine chemotherapy. However, the mechanisms underlying gastric cancer (GC) resistance to chemotherapy are still unclear. We showed that the long noncoding RNA CRNDE was related to the chemosensitivity of GC in clinical samples and a PDX model. CRNDE was decreased and inhibited autophagy flux in chemoresistant GC cells. CRNDE directly bound to splicing protein SRSF6 to reduce its protein stability and thus regulate alternative splicing (AS) events. We determined that SRSF6 regulated the PICALM exon 14 skip splice variant and triggered a significant S-to-L isoform switch, which contributed to the expression of the long isoform of PICALM (encoding PICALML). Collectively, our findings reveal the key role of CRNDE in autophagy regulation, highlighting the significance of CRNDE as a potential prognostic marker and therapeutic target against chemoresistance in GC.

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RNA-seq of HeLa cells stably overexpressing SRSF6-GFP grown under normoxic and hypoxic conditions

Project description:We used HeLa cells that overexpress GFP-tagged SRSF6 (4-fold) were grown in normal conditions (Normoxia, 21% oxygen) or hypoxic conditions (Hypoxia, 0.2% oxygen). compared the binding pattern of SRSF6 between normoxia, 4h hypoxia and 24h hypoxia.

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SRSF1 is involved in alternative mRNA splicing in granulosa cell survival

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