ArticleCell death & disease2022
Splicing factor SRSF3 represses translation of p21
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- Transcription-independent induction of rapid-onset senescence is integral to healing.Nature cell biology · 2026Article
- Regulation of oncogenic C-terminal truncated p53β protein isoform expression by SRSF3-UPF1 splicing and surveillance axis.Cell & bioscience · 2026Article
- Low hyper-oxygen exposure induces p21-dependent p53-independent senescence in alveolar cells.International journal of medical sciences · 2026Article
- SLC30A4-AS1 Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via the Alternative Splicing of TP53BP1.Cell proliferation · 2025Article
- Targeting the CLK2/SRSF9 splicing axis in prostate cancer leads to decreased ARV7 expression.Molecular oncology · 2025Article
- Factors affecting the expression and stability of full-length and truncated SRSF3 proteins in human cancer cells.Scientific reports · 2024Article
- 3'UTR Diversity: Expanding Repertoire of RNA Alterations in Human mRNAs.Molecules and cells · 2023Review
- SF3B4 Regulates Cellular Senescence and Suppresses Therapy-induced Senescence of Cancer Cells.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serine/arginine-rich splicing factor 3 (SRSF3) is an RNA binding protein that most often regulates gene expression at the splicing level. Although the role of SRSF3 in mRNA splicing in the nucleus is well known, its splicing-independent role outside of the nucleus is poorly understood. Here, we found that SRSF3 exerts a translational control of p21 mRNA. Depletion of SRSF3 induces cellular senescence and increases the expression of p21 independent of p53. Consistent with the expression patterns of SRSF3 and p21 mRNA in the TCGA database, SRSF3 knockdown increases the p21 mRNA level and its translation efficiency as well. SRSF3 physically associates with the 3'UTR region of p21 mRNA and the translational initiation factor, eIF4A1. Our study proposes a model in which SRSF3 regulates translation by interacting with eIF4A1 at the 3'UTR region of p21 mRNA. We also found that SRSF3 localizes to the cytoplasmic RNA granule along with eIF4A1, which may assist in translational repression therein. Thus, our results provide a new mode of regulation for p21 expression, a crucial regulator of the cell cycle and senescence, which occurs at the translational level and involves SRSF3.
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