Downregulation of splicing factor SRSF3 induces p53β, an alternatively spliced isoform of p53 that promotes cellular senescence
Open accessAbstract
Most human pre-mRNA transcripts are alternatively spliced, but the significance and fine-tuning of alternative splicing in different biological processes is only starting to be understood. SRSF3 (SRp20) is a member of a highly conserved family of splicing factors that have critical roles in key biological processes, including tumor progression. Here, we show that SRSF3 regulates cellular senescence, a p53-mediated process to suppress tumorigenesis, through TP53 alternative splicing. Downregulation of SRSF3 was observed in normal human fibroblasts undergoing replicative senescence, and was associated with the upregulation of p53β, an alternatively spliced isoform of p53 that promotes p53-mediated senescence. Knockdown of SRSF3 by short interfering RNA (siRNA) in early-passage fibroblasts induced senescence, which was associated with elevated expression of p53β at mRNA and protein levels. Knockdown of p53 partially rescued SRSF3-knockdown-induced senescence, suggesting that SRSF3 acts on p53-mediated cellular senescence. RNA pulldown assays demonstrated that SRSF3 binds to an alternatively spliced exon uniquely included in p53β mRNA through the consensus SRSF3-binding sequences. RNA crosslinking and immunoprecipitation assays (CLIP) also showed that SRSF3 in vivo binds to endogenous p53 pre-mRNA at the region containing the p53β-unique exon. Splicing assays using a transfected TP53 minigene in combination with siRNA knockdown of SRSF3 showed that SRSF3 functions to inhibit the inclusion of the p53β-unique exon in splicing of p53 pre-mRNA. These data suggest that downregulation of SRSF3 represents an endogenous mechanism for cellular senescence that directly regulates the TP53 alternative splicing to generate p53β. This study uncovers the role for general splicing machinery in tumorigenesis, and suggests that SRSF3 is a direct regulator of p53.
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SRSF3, a conserved splicing factor, controls production of p53β during replicative senescence.
“We recently discovered that SRSF3, a member of a highly conserved family of splicing factors, regulates the generation of p53β during replicative senescence (16).”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [16]
SRSF3 was downregulated in CD28-CD57+ subsets.
“SRSF3, a splicing factor that restricts the alternative splicing generating p53β (16), was downregulated in the CD28 -CD57 + subsets (Figure 2D and Supplemental Figure 5F), consistent with the increased p53β mRNA (Figure 2C).”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [16]
The change in Δ133p53 occurs at the protein level, not the mRNA level, in both CD8+ T lymphocytes and fibroblasts.
“p53β is likely to be regulated by SRSF3-mediated alternative splicing in both cell types (16), and the change in Δ133p53 occurs at the protein level, but not the mRNA level, in both cell types.”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [16]
p53β is likely regulated by SRSF3-mediated alternative splicing in both CD8+ T lymphocytes and fibroblasts.
“p53β is likely to be regulated by SRSF3-mediated alternative splicing in both cell types (16), and the change in Δ133p53 occurs at the protein level, but not the mRNA level, in both cell types.”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [16]
The level of splicing factor SRSF3 decreases in replicatively senescent human fibroblasts, and its knockdown promotes p53-mediated senescence by directly upregulating p53β.
“For example, the level of the splicing factor SRSF3 decreases in replicatively senescent human fibroblasts, and its knockdown promotes p53-mediated senescence by directly upregulating p53β, an alternatively spliced p53 isoform [201].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [201]
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- Authors
- Tang, Y., Horikawa, I., Ajiro, M., Robles, A. I., Fujita, K., Mondal, A. M., Stauffer, J. K., Zheng, Z.-M., & Harris, C. C.
- Affiliations
- National Institutes of Health (US)
- National Cancer Institute (US)
- Corresponding author
- Harris, C C
- Venue
- Oncogene
- Published
- 2012-07-09
- Volume
- 32
- Issue
- 22
- Pages
- 2792-2798
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC6503963
- OpenAlex
- W1990628815
- Cited by
- 165
- References
- 75
- Citations by year
- 2026: 12 · 2025: 5 · 2024: 18 · 2023: 11 · 2022: 16 · 2021: 19 · 2020: 13 · 2019: 9 · 2018: 16 · 2017: 9 · 2016: 9 · 2015: 9 · 2014: 10 · 2013: 9
- FWCI
- 3.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01BC005795)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- SRSF3, SRp20, cellular senescence, replicative senescence, splicing factors, carcinogenesis, fibroblasts, p53 isoforms
- MeSH terms
- Serine-Arginine Splicing Factors, Cell Line, Cell Transformation, Neoplastic, Fibroblasts, Humans, RNA Precursors, RNA, Messenger, Down-Regulation, Up-Regulation, Tumor Suppressor Protein p53, RNA-Binding Proteins, Cellular Senescence, Alternative Splicing, Protein Isoforms, RNA Interference, RNA, Small Interfering
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