Abstract
Gastric cancer (GC) represents a prevalent form of malignant neoplasm characterized by elevated incidence and fatality rates, limited early detection capabilities, and unfavorable clinical outcomes. Its occurrence and development involve complex biological processes. As a recently identified form of cellular demise, ferroptosis has been observed across multiple cancer types, garnering significant research interest in contemporary studies. Nevertheless, the precise regulatory networks governing ferroptosis in gastric cancer, along with its functional implications in the initiation and advancement of this malignancy, remain unclear. This study seeks to elucidate the functional significance of ferroptosis in the pathogenesis of GC, systematically review the dysregulated metabolic pathways associated with this cell death process, and elucidate the intricate interactions among ferroptosis-related signaling cascades. These investigations are expected to establish a novel conceptual framework for understanding the molecular pathogenesis of gastric cancer and identifying potential therapeutic interventions. A comprehensive literature search was conducted using PubMed to identify relevant original research articles and review papers examining the molecular mechanisms underlying ferroptosis in gastric carcinoma. The search strategy incorporated the following key terms: "Ferroptosis," "Ferroptosis and gastric cancer," "Ferroptosis and GSH," "Ferroptosis and GPX4," "Ferroptosis and system Xc-," "Iron metabolism," "lipid peroxidation," "FSP1-CoQ10," "DHODH-CoQH2," "GCH1-BH4," "ferroptosis inducer," etc. Emerging evidence from contemporary research indicates that targeted ferroptosis represents a novel and potentially efficacious treatment modality for patients with gastric cancer. Along with the identification of precise molecular targets for therapeutic intervention, the metabolic regulatory networks associated with ferroptosis remains an essential area for future research endeavors.