ArticleMolecular cancer2015
Serine/arginine-rich splicing factor 3 (SRSF3) regulates homologous recombination-mediated DNA repair.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- Interplay of telomerase non-canonical functions in NK cell resistance to iCasp9-mediated apoptosis.Cell death discovery · 2026Article
- SRSF3-TRIM28-MDC1 prevents DNA damage caused by R-loops in fatty liver disease in mice.JCI insight · 2026Article
- LnCeVar 2.0: an updated resource and web tools for genomic variations disrupting ceRNA networks from single-cell/spatial transcriptomics data.Nucleic acids research · 2026Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- Article
- NLRP7 maintains the genomic stability during early human embryogenesis via mediating alternative splicing.Communications biology · 2025Article
- Function of serine/arginine-rich splicing factors in hematopoiesis and hematopoietic malignancies.Cancer cell international · 2024Review
- Factors affecting the expression and stability of full-length and truncated SRSF3 proteins in human cancer cells.Scientific reports · 2024Article
- The Many Roads from Alternative Splicing to Cancer: Molecular Mechanisms Involving Driver Genes.Cancers · 2024Review
- Characterization of alternative splicing events and prognostic signatures in gastric cancer.Cancer cell international · 2024Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- Splicing factor BUD31 promotes ovarian cancer progression through sustaining the expression of anti-apoptotic BCL2L12.Nature communications · 2022Article
- Hepatocyte Deletion of IGF2 Prevents DNA Damage and Tumor Formation in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Biological function and molecular mechanism of SRSF3 in cancer and beyond.Oncology letters · 2022Review
- SRSF3 Restriction Eases Cervical Cancer Cell Viability and Metastasis via Adjusting PI3K/AKT/mTOR Signaling Pathway.Contrast media & molecular imaging · 2022Article
- RBM6 splicing factor promotes homologous recombination repair of double-strand breaks and modulates sensitivity to chemotherapeutic drugs.Nucleic acids research · 2021Article
- KDM3A regulates alternative splicing of cell-cycle genes following DNA damage.RNA (New York, N.Y.) · 2021Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOur previous work found that serine/arginine-rich splicing factor 3 (SRSF3) was overexpressed in human ovarian cancer and the overexpression of SRSF3 was required for ovarian cancer cell growth and survival. The mechanism underlying the role of SRSF3 in ovarian cancer remains to be addressed.
methodsWe conducted microarray analysis to profile the gene expression and splicing in SRSF3-knockdown cells and employed quantitative PCR and western blotting to validate the profiling results. We used chromatin immunoprecipitation to study transcription and the direct repeat green fluorescent protein reporter assay to study homologous recombination-mediated DNA repair (HRR).
resultsWe identified 687 genes with altered expression and 807 genes with altered splicing in SRSF3-knockdown cells. Among expression-altered genes, those involved in HRR, including BRCA1, BRIP1 and RAD51, were enriched and were all downregulated. We demonstrated that the downregulation of BRCA1, BRIP1 and RAD51 expression was caused by decreased transcription and not due to increased nonsense-mediated mRNA decay. Further, we found that SRSF3 knockdown impaired HRR activity in the cell and increased the level of γ-H2AX, a biomarker for double-strand DNA breaks. Finally, we observed that SRSF3 knockdown changed splicing pattern of KMT2C, a H3K4-specific histone methyltransferase, and reduced the levels of mono- and trimethylated H3K4.
conclusionThese results suggest that SRSF3 is a new regulator of HRR process, which possibly regulates the expression of HRR-related genes indirectly through an epigenetic pathway. This new function of SRSF3 not only explains why overexpression of SRSF3 is required for ovarian cancer cell growth and survival but also offers a new insight into the mechanism of the neoplastic transformation.
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