Sep 2026· Journal of Cancer· Vol 17, pp. 1808 - 1820· 0 citations· 134 references
Medicine
TL;DR
This review synthesizes the molecular mechanisms of mitophagy, its crosstalk with ferroptosis, and its context dependent roles in breast cancer development, with the aim of offering therapeutic insights that may inform breast cancer treatment.
Abstract
Breast cancer remains the most commonly diagnosed malignancy among women worldwide and a leading cause of cancer related mortality in this population. Mitochondrial dysfunction is increasingly recognized as a hallmark of breast cancer, contributing to tumor initiation, progression, and therapeutic resistance. Mitophagy, a selective form of autophagy that eliminates damaged or dysfunctional mitochondria, is essential for maintaining cellular and mitochondrial homeostasis. Accumulating evidence indicates that mitophagy plays a context dependent role in breast cancer. Impaired mitophagy permits the accumulation of damaged mitochondria and promotes tumor growth, migration, and invasion, whereas appropriately activated mitophagy removes damaged mitochondria and suppresses tumor progression. This review synthesizes the molecular mechanisms of mitophagy, its crosstalk with ferroptosis, and its context dependent roles in breast cancer development, with the aim of offering therapeutic insights that may inform breast cancer treatment.
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