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Figure 1. Mechanisms of EMF Regulation in Prostate Cancer: Calcium Signaling, Extracellular Vesicle Reprogramming, and Ferroptosis Modulation. (A) Calcium signaling as the central nodal effector. EMFs induce piezoelectric effects in prostatic calcium/phosphate crystals, generating mechanical stress that activates VGCCs, thereby initiating extracellular Ca²⁺ influx and intracellular signaling cascades, such as calcium-induced calcium release (CICR). EMFs (Low-Frequency) amplify this process, driving mitochondrial membrane depolarization and ROS overproduction, which synergizes with iron-dependent lipid peroxidation to potentiate ferroptosis; (B) Frequency-dependent ferroptosis modulation. EMFs (Low-Frequency) promote ferroptosis via the Ca²⁺-ROS-Fe²⁺ axis, inducing lipid peroxidation and oxidative damage. Terahertz Waves (34.5 THz) suppress ferroptosis by inhibiting iron-transferrin binding; (C) EMFs-driven reprogramming of EVs to promote metastasis. EMFs (Low-Frequency) exposure triggers Ca²⁺-dependent EV biogenesis and cargo sorting, enriching pro-metastatic proteins (e.g., MMP2/MMP9) and altering miRNA profiles (upregulate oncogenic miR-155/-21/-210 and suppress tumor-suppressive miR-126/-200c). These EVs enhance basement membrane invasion and metastatic dissemination through MMP-mediated extracellular matrix degradation and miRNA-driven epigenetic remodeling. VGCC: Voltage-gated Ca²⁺ channels; EMFs: electromagnetic fields; EV: Extracellular vesicle; TF: transferrin; TFR: transferrin receptor; ROS: reactive oxygen species; MMP: matrix Metalloproteinase.