Overview
- NKAPL overexpression in mouse xenograft models resulted in significantly smaller tumors and reduced lung metastases.
- Mechanistic studies show NKAPL binds to and stabilizes TRIM21, diminishing p65 phosphorylation and suppressing NF-κB-driven inflammatory signaling.
- Restoration of NKAPL expression in NSCLC cell lines induced apoptosis, cell cycle arrest, and inhibited proliferation, migration and invasion.
- Frequent promoter hypermethylation of NKAPL in patient tumor samples underscores its utility as a potential diagnostic biomarker.
- Investigators propose developing demethylation-based therapies to reactivate NKAPL and disrupt NF-κB-mediated cancer progression in clinical settings.