Unleashing the potential of ferroptosis, autophagy, and mitochondrial dynamics as emerging modalities in cancer treatment

Abstract

New approaches in cancer treatment are increasingly emphasizing innovative biological processes such as ferroptosis, autophagy, and mitochondrial dynamics. Ferroptosis, characterized by iron-dependent lipid peroxidation, has emerged as a promising strategy for targeting aggressive and metastatic cancers including those of the lung, breast, prostate, pancreas, and colorectal regions. Autophagy, a cellular degradation mechanism, plays a dual role in cancer—it can inhibit tumor development by clearing damaged cellular components or, paradoxically, support tumor growth under stressful conditions. Mitochondrial dynamics, encompassing the continuous processes of fission and fusion, are often disrupted in various types of human cancers, leading to altered metabolism, therapy resistance, and metastasis. These disruptions make them favorable targets for innovative treatments. This review highlights ferroptosis as a novel form of cell death, focusing on its biological pathways and connections with mitochondrial dysfunction and autophagy. Understanding the interplay among these three mechanisms in the complex biology of cancer could provide a more comprehensive and effective approach to cancer therapy.

Keywords: Ferroptosis; Autophagy; Mitochondrial dynamics; Cancer treatment; Regulated cell death

Core Tip: This review explores the emerging therapeutic potential of ferroptosis, autophagy, and mitochondrial dynamics in cancer treatment. By targeting ferroptosis—an iron-dependent form of cell death—alongside the modulation of autophagy and mitochondrial function, novel strategies can be developed to overcome cancer cell resistance and metastasis. Understanding the intricate interplay among these processes offers a promising avenue for more effective and personalized cancer therapies.