Cuproptosis in lung cancer: a nexus of ncRNA regulation, epigenetics, and tumor microenvironment Remodeling

Lung cancer remains a leading cause of cancer-related mortality worldwide. Cuproptosis, a new form of programmed cell death, is emerging as a key regulator in tumor progression. In this review, we talk about the interplay between cuproptosis, non-coding RNAs (ncRNAs), and epigenetic modifications in lung cancer. We performed an extensive review of recent literature to explore the function of ncRNAs in the regulation of cuproptosis, their effects on tumor microenvironment remodeling, immune response regulation, and drug sensitivity. ncRNAs were found to modulate cuproptosis by influencing copper metabolism, apoptosis, and oxidative stress response. Specific ncRNA signatures possess prognostic biomarker and therapeutic target potential in lung cancer. In addition, ncRNA-mediated epigenetic regulation has significant influence on deciding lung cancer formation and treatment outcome. The integration of non-coding RNAs related to cuproptosis into therapies offers great promise for the improvement of lung cancer prognosis. Further studies are needed to validate these findings and promote their implementation in clinical practice.