SYT8 Drives Colorectal Cancer Progression and Immune Evasion via the SETD1A-H3K4me3 Axis - PubMed
6 hours ago
- #Epigenetics
- #Immunotherapy
- #Colorectal Cancer
- SYT8 is significantly upregulated in colorectal cancer tumors and predicts poor prognosis.
- SYT8 expression is primarily in tumor cell nuclei and promotes cancer cell proliferation and invasion.
- SYT8 depletion reduces while overexpression enhances CRC progression and epithelial-mesenchymal transition (EMT).
- SYT8 interacts directly with SETD1A, forming a positive-feedback loop that increases H3K4me3 levels.
- The SYT8-SETD1A axis activates pro-tumorigenic genes, driving cell cycle and EMT.
- High SYT8 expression correlates with increased regulatory T-cell infiltration, suggesting immune evasion and potential immunotherapy resistance.
- SYT8 promotes CRC progression via SETD1A/H3K4me3-mediated activation, EMT induction, and immune microenvironment remodeling.
- SYT8 is established as a prognostic biomarker and therapeutic target in colorectal cancer.