ArticleCellular and molecular life sciences : CMLS2020
Modulation of SRSF2 expression reverses the exhaustion of TILs via the epigenetic regulation of immune checkpoint molecules.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Regulation of immune checkpoint molecules in cancer immune evasion and therapy.Nature reviews. Cancer · 2026Review
- Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.Nature communications · 2026Article
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- NEAT1 is a therapeutic target for reversing T-cell exhaustion in bladder cancer.Journal for immunotherapy of cancer · 2025Article
- The epigenetic hallmarks of immune cells in cancer.Molecular cancer · 2025Review
- Epigenetic Regulation of Stromal and Immune Cells and Therapeutic Targets in the Tumor Microenvironment.Biomolecules · 2025Review
- Tumor-promoting effect and tumor immunity of SRSFs.Frontiers in cell and developmental biology · 2025Review
- Biological functions of 5-methylcytosine RNA-binding proteins and their potential mechanisms in human cancers.Frontiers in oncology · 2025Review
- Article
- BTLA biology in cancer: from bench discoveries to clinical potentials.Biomarker research · 2024Review
- PABPN1 functions as a predictive biomarker in colorectal carcinoma.Molecular biology reports · 2023Article
- SRSF2 is required for mRNA splicing during spermatogenesis.BMC biology · 2023Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Essential role of bromodomain proteins in renal cell carcinoma (Review).Molecular medicine reports · 2023Review
- Hypoxia-induced loss of SRSF2-dependent DNA methylation promotes CTCF-mediated alternative splicing of VEGFA in breast cancer.iScience · 2023Article
- Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Non-coding RNAs: Key players in T cell exhaustion.Frontiers in immunology · 2022Review
- Speckles and paraspeckles coordinate to regulate HSV-1 genes transcription.Communications biology · 2021Article
- A four-genes based diagnostic signature for osteoarthritis.Rheumatology international · 2021Article
- How metabolism bridles cytotoxic CD8Trends in immunology · 2021Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The elevated expression of immune checkpoints by the tumor microenvironment is associated with poor prognosis in several cancers due to the exhaustion of tumor-infiltrating lymphocytes (TILs), and the effective suppression of the expression of these genes is key to reversing the exhaustion of TILs. Herein, we determined that serine/arginine-rich splicing factor 2 (SRSF2) is a target for blocking the tumor microenvironment-associated immunosuppressive effects. We found that the expression of SRSF2 was increased in exhausted T cells and that SRSF2 was involved in multiple immune checkpoint molecules mediating TILs' exhaustion. Furthermore, SRSF2 was revealed to regulate the transcription of these immune checkpoint genes by associating with an acyl-transferases P300/CBP complex and altering the H3K27Ac level near these genes, thereafter influencing the recruitment of signal transducer and activator of transcription 3 (STAT3) to these gene promoters. Collectively, our data indicated that SRSF2 functions as a modulator of the anti-tumor response of T cells and may be a therapeutic target for reversing the exhaustion of TILs.
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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.