Regulation of cisplatin resistance in lung cancer by epigenetic mechanisms

Lung cancer remains one of the most prevalent and lethal malignancies worldwide, responsible for nearly 1.8 million deaths annually, which accounts for approximately 18.7% of global cancer-related mortality. Cisplatin, a highly effective and widely utilized anticancer drug, is particularly effective against solid tumors and serves as a cornerstone of adjuvant chemotherapy for lung cancer. Despite continuous optimization of cisplatin-based chemotherapy regimens, the emergence of cisplatin resistance frequently results in treatment failure, significantly limiting its clinical utility and therapeutic efficacy. To address this challenge, researchers have extensively investigated the biological mechanisms underlying cisplatin resistance, including impaired DNA repair pathways and inhibition of apoptosis. Among these mechanisms, epigenetic regulation-encompassing DNA methylation, histone modifications, and noncoding RNA (ncRNA) regulation-has emerged as a critical factor in mediating cisplatin resistance by modulating gene expression and signaling pathways. This review comprehensively explores the role of epigenetic mechanisms in cisplatin resistance in lung cancer, highlighting recent research findings and their potential implications for developing strategies to overcome drug resistance.