SLC12A8 Drives Immune Evasion and Metastasis in Luminal B Breast Cancer by Inducing CD8+ T-Cell Exhaustion via the TLR Signaling Pathway - PubMed
4 days ago
- #TLR Signaling
- #Immune Evasion
- #Breast Cancer
- SLC12A8 is significantly upregulated in Luminal B breast cancer and correlates with poor prognosis.
- SLC12A8 induces CD8+ T-cell exhaustion via the TLR signaling pathway, leading to immune evasion and metastasis.
- Knockdown of SLC12A8 or inhibition of the TLR pathway reverses CD8+ T-cell exhaustion and reduces cancer cell invasion.
- Bioinformatic and experimental analyses confirm SLC12A8's role in reducing CD8+ T-cell infiltration and function in the tumor microenvironment.
- SLC12A8's activation of the TLR pathway upregulates PD-1 on CD8+ T cells, promoting their exhaustion and enhancing cancer cell invasiveness.
- SLC12A8 overexpression in normal breast epithelial cells mimics the exhausted T-cell phenotype, suggesting its potential as a therapeutic target.