ArticleRSC advances2018
Inhibition of the expression of oncogene SRSF3 by blocking an exonic splicing suppressor with antisense oligonucleotides.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- Genomic landscape and tumor immune microenvironment of osteosarcoma: Bridging mechanistic insights to precision therapeutics.Bone reports · 2026Review
- Disease-driven post-transcriptional alterations and alternative splicing in podocytes in focal segmental glomerulosclerosis.EMBO molecular medicine · 2026Article
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- RNA splicing in cancer cell death regulation: shedding light on the molecular mechanisms and potential clinical applications.Cell death & disease · 2026Review
- Synthetic-polymer-assisted antisense oligonucleotide delivery: targeted approaches for precision disease treatment.Beilstein journal of nanotechnology · 2025Review
- SR proteins in cancer: function, regulation, and small inhibitor.Cellular & molecular biology letters · 2024Review
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- Emerging roles of alternative RNA splicing in oral squamous cell carcinoma.Frontiers in oncology · 2022Review
- Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- Poison Exon Splicing Regulates a Coordinated Network of SR Protein Expression during Differentiation and Tumorigenesis.Molecular cell · 2020Article
- Serine/Arginine-Rich Splicing Factor 3 Modulates the Alternative Splicing of Cytoplasmic Polyadenylation Element Binding Protein 2.Molecular cancer research : MCR · 2019Article
- Inclusion of hnRNP L Alternative Exon 7 Is Associated with Good Prognosis and Inhibited by Oncogene SRSF3 in Head and Neck Squamous Cell Carcinoma.BioMed research international · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antisense oligonucleotides (ASOs) have been widely used to regulate alternative splicing of pre-mRNA by targeting splice sites, branch points, or exonic splice enhancers to increase exon skipping or intron retention. So far, few studies have used ASOs to block exonic splicing suppressor (ESS) and increase exon inclusion. Previously, we demonstrated that serine and arginine rich splicing factor 3 (SRSF3) (also called SRp20) is an oncogene. The inclusion of its alternative exon 4 down-regulates its expression. An ESS motif is responsible for the skipping of alternative exon 4. Here, we used an economical method to screen effective anti-ESS ASO. We discovered that an ASO targeting the ESS motif can promote the inclusion of exon 4, reduce SRSF3 expression, and inhibit cell growth in oral cancer cells. Our results suggested that using anti-ESS ASOs can efficiently increase exon inclusion and be used as a potential anti-cancer drug.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.