This review examines how mitochondrial dysfunction linked to reactive oxygen species affects tumour growth and metastasis in malignant melanoma, indicating potential therapeutic targets.
Reactive oxygen species (ROS) are critical to cellular metabolism, signal transduction and apoptosis. Recent studies have revealed the dual role of ROS in malignant melanoma pathogenesis and progression, where they can both promote tumour proliferation and metastasis or inhibit tumour growth by inducing apoptosis. Mitochondria, often referred to as the energy factories of cells, are closely involved in ROS generation, and their dysfunction significantly affects cellular homeostasis. This review explores the mechanisms by which ROS-mediated mitochondrial dysfunction contributes to malignant melanoma, focusing on its effects within the tumour microenvironment and its potential as a therapeutic target. Understanding these interactions is essential for developing novel strategies to combat malignant melanoma.
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Li et al. (2025) studied this question.
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