Revealing the Key Redox Regulatory Mechanisms of ERO1A in Cancer Progression and Its Therapeutic Prospects

Oxidative stress plays a dual role in cancer, influencing both tumor promotion and suppression through reactive oxygen species (ROS) regulation. Cancer cells upregulate antioxidant systems, evade ROS-induced cell death, and use ROS signaling to drive tumor progression and immune evasion. ERO1A (Endoplasmic Reticulum Oxidoreductase 1 Alpha), a key enzyme in redox homeostasis, is highly expressed in various cancers and has been implicated in enhancing ROS levels, thereby promoting tumor growth, metabolic reprogramming, and immune escape.This study systematically analyzed ERO1A expression across multiple cancer types using TCGA data. ERO1A was found to be significantly upregulated in cancers such as breast, liver, and lung adenocarcinoma, and its expression was correlated with poor patient survival. Functional analysis revealed that ERO1A regulates critical oxidative stress-related pathways, including lipid metabolism and the cytochrome P450 pathway, suggesting a central role in tumor cell adaptation to oxidative environments. Additionally, ERO1A's high expression was associated with increased immune-suppressive cell infiltration, supporting its role in promoting immune evasion and highlighting ERO1A as a potential diagnostic and prognostic marker in ROS-dependent cancers. By targeting the ERO1A-mediated redox balance, novel therapeutic strategies can be developed to counteract cancer progression. These results offer new insights into the interplay between oxidative stress and cancer, with ERO1A at the center of redox regulation.