# Dysregulation of SRSF11 in Cancer: Mechanistic Insights and Biomarker Potential for Diagnosis and Therapy

## TL;DR

This paper reviews how SRSF11, an RNA-binding protein, contributes to cancer progression and its potential as a biomarker for diagnosis and treatment.

## Contribution

The paper provides a comprehensive review of SRSF11's cancer-specific roles and regulatory mechanisms across multiple malignancies.

## Key findings

- SRSF11 is involved in cell-cycle regulation and EMT through cancer-specific signaling pathways.
- SRSF11 shows potential as a cancer-specific biomarker rather than a universal oncogenic driver.
- The paper identifies regulatory circuits involving SRSF11 in colorectal, gastric, and hepatocellular cancers.

## 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.