Exploring the Role of Cuprotosis-Associated Genes in Cancer Progression and Therapy Resistance: A Comprehensive Analysis across Multiple Cancer Types

This review presents a comprehensive overview of the role of cuprotosis-associated genes in various cancer types, highlighting their significance in tumor progression and therapy resistance. In breast cancer and colorectal cancer (CRC), dysregulation of genes involved in mitochondrial function and copper metabolism, such as FDX1, LIAS, LIPT1, DLD, DLAT, and PDHA1/PDHB, promotes metabolic reprogramming and enhances cancer cell survival. Ovarian cancer exhibits unique dysregulations in genes like ATP7B, CCS, and COMMD1, influencing copper metabolism and redox signaling pathways, thereby contributing to chemoresistance and tumor growth. Head and neck cancer involves upregulation of MT1X, ATP7A, and CCS, potentially aiding cancer cell survival under oxidative stress conditions. Lung cancer is characterized by distinct dysregulation of genes like SLC31A1, ATOX1, and COMMD1, modulating copper homeostasis and redox signaling to support tumor proliferation. Liver cancer and kidney cancer each present unique sets of dysregulated cuprotosis-associated genes, such as SLC39A4, SCO2, and ATP7A, suggesting novel therapeutic targets specific to these cancer types. Pathway analysis reveals enrichment in mineral absorption pathways, emphasizing the importance of these genes in maintaining cellular mineral homeostasis. Understanding the intricate interplay between cuprotosis-associated genes and cancer biology offers insights into potential therapeutic strategies targeting copper metabolism for improved treatment outcomes across various cancer types.