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Dysregulation of SRSF11 in Cancer: Mechanistic Insights and Biomarker Potential for Diagnosis and Therapy
Yang Jun1,2, Liu Shanshan3, Xiao Jingwen3
1Department of Laboratory Medicine, Guilin people's Hospital, No.12 Wenming Road, Guilin, Guangxi, China, 541002.
Abstract:
Serine/arginine-rich splicing factor 11 (SRSF11) is an RNA-binding regulator that modulates alternative splicing and RNA metabolism in a context-dependent manner across selected malignancies. Evidence from colorectal, hepatocellular, gastric, glioma, and a few other cancers indicates that SRSF11 participates in cell-cycle regulation, telomerase recruitment, and epithelial-mesenchymal transition (EMT) through specific signaling axes, including PAK5-SRSF11-HSPA12A in colorectal cancer, METTL3-SRSF11 in gastric and breast cancers, and SRSF11-CDK1/telomerase circuits in hepatocellular carcinoma. These mechanisms highlight SRSF11 as a candidate biomarker for diagnosis and prognosis rather than a universal oncogenic driver. We summarize the current mechanistic, post-translational, and non-coding RNA-mediated regulatory evidence, clarify the limitations of existing data, and propose future multi-omics and functional approaches to validate SRSF11-directed splicing therapy. This review integrates mechanistic insight with clinical evidence while emphasizing cancer-specific rather than generalized conclusions.
Insights
Serine/arginine-rich splicing factor 11 (SRSF11) is an RNA-binding protein involved in cancer. While not a universal driver, SRSF11 acts as a potential biomarker for diagnosis and prognosis in various cancers.
Area of Science:
- Molecular Biology
- Cancer Research
- RNA Biology
Background:
- Serine/arginine-rich splicing factor 11 (SRSF11) is an RNA-binding protein regulating alternative splicing and RNA metabolism.
- SRSF11's role is context-dependent and has been implicated in various malignancies.
Purpose of the Study:
- To review the mechanistic, post-translational, and non-coding RNA-mediated regulation of SRSF11 in cancer.
- To clarify limitations in current data and propose future research directions.
- To emphasize cancer-specific roles of SRSF11 rather than generalized conclusions.
Main Methods:
- Literature review of existing mechanistic and clinical evidence.
- Analysis of SRSF11's involvement in signaling pathways (e.g., PAK5-SRSF11-HSPA12A, METTL3-SRSF11, SRSF11-CDK1/telomerase).
- Identification of SRSF11's participation in cell-cycle regulation, telomerase recruitment, and epithelial-mesenchymal transition (EMT).
Main Results:
- SRSF11 participates in key cancer-related processes like cell-cycle regulation, telomerase recruitment, and EMT.
- Specific signaling axes involving SRSF11 have been identified in colorectal, gastric, breast, and hepatocellular cancers.
- SRSF11 functions as a context-dependent regulator, suggesting its potential as a cancer biomarker.
Conclusions:
- SRSF11 is a potential biomarker for cancer diagnosis and prognosis, not a universal oncogenic driver.
- Further multi-omics and functional studies are needed to validate SRSF11-directed splicing therapy.
- Understanding cancer-specific roles of SRSF11 is crucial for therapeutic development.
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