Publication Details
Abstract
Ferritin, a highly conserved intracellular iron-storage protein, has emerged as a multifunctional biomarker beyond its classical role in iron homeostasis. Increasing evidence indicates that ferritin acts as a key mediator at the intersection of iron metabolism, inflammation, oxidative stress, and tumor biology. In solid tumors, elevated serum ferritin levels have been consistently associated with tumor progression, systemic inflammation, immune dysregulation, and poor clinical outcomes. Mechanistically, ferritin contributes to tumor growth by modulating iron availability, promoting reactive oxygen species (ROS) generation, enhancing angiogenesis, and influencing immune cell polarization within the tumor microenvironment. Pro-inflammatory cytokines such as IL-6 and TNF-α upregulate ferritin expression, further linking chronic inflammation to carcinogenesis and tumor aggressiveness. Clinically, hyperferritinemia has been reported in various solid malignancies, including hepatocellular carcinoma, breast cancer, lung cancer, colorectal cancer, and pancreatic cancer, where it correlates with advanced stage, metastasis, chemoresistance, and reduced overall survival. Furthermore, ferritin has shown potential utility as a prognostic indicator and as a complementary marker alongside established tumor biomarkers. This narrative review synthesizes current evidence on the biological functions of ferritin in cancer-related inflammation and evaluates its diagnostic and prognostic value across major solid tumors. Understanding the dual role of ferritin as both an inflammatory mediator and a tumor-associated biomarker may provide new insights into risk stratification, therapeutic monitoring, and potential iron-targeted treatment strategies in oncology.