ArticleNature communications2018
Mutually exclusive acetylation and ubiquitylation of the splicing factor SRSF5 control tumor growth.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed.
- Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- MRPL12 K163 acetylation inhibits ccRCC via driving mitochondrial metabolic reprogramming.Cell death & disease · 2025Article
- SRSF3 undergoes phase separation in lung cancer and is associated with immunity and ferroptosis.Scientific reports · 2025Article
- Acetylation: a new target for protein degradation in cancer.Trends in cancer · 2025Review
- APlants (Basel, Switzerland) · 2025Article
- Targeting SRSF10 might inhibit M2 macrophage polarization and potentiate anti-PD-1 therapy in hepatocellular carcinoma.Cancer communications (London, England) · 2024Article
- Substrate and Functional Diversity of Protein Lysine Post-translational Modifications.Genomics, proteomics & bioinformatics · 2024Review
- hGRAD: A versatile "one-fits-all" system to acutely deplete RNA binding proteins from condensates.The Journal of cell biology · 2024Article
- LINC01852 inhibits the tumorigenesis and chemoresistance in colorectal cancer by suppressing SRSF5-mediated alternative splicing of PKM.Molecular cancer · 2024Article
- Comprehensive analysis of splicing factor SRs-related gene characteristics: predicting osteosarcoma prognosis and immune regulation status.Frontiers in oncology · 2024Article
- Article
- Splicing alterations in pancreatic ductal adenocarcinoma: a new molecular landscape with translational potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Research Progress in Function and Regulation of E3 Ubiquitin Ligase SMURF1.Current medical science · 2023Review
- The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- SRSF3/AMOTL1 splicing axis promotes the tumorigenesis of nasopharyngeal carcinoma through regulating the nucleus translocation of YAP1.Cell death & disease · 2023Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Targeting fibrinogen-like protein 1 enhances immunotherapy in hepatocellular carcinoma.The Journal of clinical investigation · 2023Article
- SRSF5 Regulates the Expression of BQ323636.1 to Modulate Tamoxifen Resistance in ER-Positive Breast Cancer.Cancers · 2023Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most tumor cells take up more glucose than normal cells. Splicing dysregulation is one of the molecular hallmarks of cancer. However, the role of splicing factor in glucose metabolism and tumor development remains poorly defined. Here, we show that upon glucose intake, the splicing factor SRSF5 is specifically induced through Tip60-mediated acetylation on K125, which antagonizes Smurf1-mediated ubiquitylation. SRSF5 promotes the alternative splicing of CCAR1 to produce CCAR1S proteins, which promote tumor growth by enhancing glucose consumption and acetyl-CoA production. Conversely, upon glucose starvation, SRSF5 is deacetylated by HDAC1, and ubiquitylated by Smurf1 on the same lysine, resulting in proteasomal degradation of SRSF5. The CCAR1L proteins accumulate to promote apoptosis. Importantly, SRSF5 is hyperacetylated and upregulated in human lung cancers, which correlates with increased CCAR1S expression and tumor progression. Thus, SRSF5 responds to high glucose to promote cancer development, and SRSF5-CCAR1 axis may be valuable targets for cancer therapeutics.
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