ArticleJournal of experimental & clinical cancer research : CR2021
Splicing factors control triple-negative breast cancer cell mitosis through SUN2 interaction and sororin intron retention.
Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
- SNRPD2-CPSF7-UBE2K axis drives ovarian cancer progression via alternative splicing-polyadenylation crosstalk.Oncogene · 2026Article
- Interplay of telomerase non-canonical functions in NK cell resistance to iCasp9-mediated apoptosis.Cell death discovery · 2026Article
- Modulation of splicing factors SF3B1 and SRSF1 by polypurine reverse Hoogsteen hairpins affects the splicing pattern of estrogen receptor α in breast cancer cells.Cancer cell international · 2026Article
- Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SNRPD2-mediated regulation of DDX39B splicing promotes endometrial cancer progression by suppressing the activation of CTSC cryptic exons.Cell death & disease · 2026Article
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- Reference-free RNA profiling predicts triple negative breast cancer chemoresistance to neoadjuvant treatment.NAR cancer · 2025Article
- SF3B6 promotes the oncogenic phenotypes of MDA-MB-231 cells by extensively interacting with and regulating transcripts expression and alternative splicing.Scientific reports · 2025Article
- Pharmacological CLK inhibition disrupts SR protein function and RNA splicing blocking cell growth and migration in TNBC.Breast cancer research : BCR · 2025Article
- Metabolic reprogramming and prognostic insights in molecular landscapes driven by glycolysis in ovarian cancer.Scientific reports · 2025Article
- Pogo transposons provide tools to restrict cancer growth.Molecular oncology · 2025Article
- Review
- E2F1-mediatedCytoJournal · 2025Article
- Evaluation of Spliceosome Protein SmD2 as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2024Article
- Molecular interplay between the upregulated levels of Sad1 and UNC84 Domain Containing 2 (SUN2) and gene expression in medulloblastoma cells.Molecular biology reports · 2024Article
- Altered methylation of imprinted genes in neuroblastoma: implications for prognostic refinement.Journal of translational medicine · 2024Article
- Article
- Identification of Genes Hub Associated with Triple-Negative Breast Cancer and Cannabidiol Analogs Potential Inhibitory Agents: An In-silico Study.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Synthetic Lethality between Cohesin and WNT Signaling Pathways in Diverse Cancer Contexts.Cells · 2024Article
- The synergism of SMC1A cohesin gene silencing and bevacizumab against colorectal cancer.Journal of experimental & clinical cancer research : CR · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic opportunities. Recently, splicing factors have gained attention as potential targets for cancer treatment. Here we systematically evaluated the role of RNA splicing factors in TNBC cell proliferation.
methodsIn this study, we performed an RNAi screen targeting 244 individual splicing factors to systematically evaluate their role in TNBC cell proliferation. For top candidates, mechanistic insight was gained using amongst others western blot, PCR, FACS, molecular imaging and cloning. Pulldown followed by mass spectrometry were used to determine protein-protein interactions and patient-derived RNA sequencing data was used relate splicing factor expression levels to proliferation markers.
resultsWe identified nine splicing factors, including SNRPD2, SNRPD3 and NHP2L1, of which depletion inhibited proliferation in two TNBC cell lines by deregulation of sister chromatid cohesion (SCC) via increased sororin intron 1 retention and down-regulation of SMC1, MAU2 and ESPL1. Protein-protein interaction analysis of SNRPD2, SNRPD3 and NHP2L1 identified that seven out of the nine identified splicing factors belong to the same spliceosome complex including novel component SUN2 that was also critical for efficient sororin splicing. Finally, sororin transcript levels are highly correlated to various proliferation markers in BC patients.
conclusionWe systematically determined splicing factors that control proliferation of breast cancer cells through a mechanism that involves effective sororin splicing and thereby appropriate sister chromatid cohesion. Moreover, we identified SUN2 as an important new spliceosome complex interacting protein that is critical in this process. We anticipate that deregulating sororin levels through targeting of the relevant splicing factors might be a potential strategy to treat TNBC.
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