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Cancer Cells and Metastasis / Cancer, Hypoxia, and Metabolism · Journal article
Stem Cells · August 13, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review exploring the interconnected roles of mitochondrial dynamics and ion signalling in cancer stem cell metabolism and therapy resistance. It synthesizes mechanistic concepts and identifies therapeutic opportunities but does not report original data, clinical trials, or evidence synthesis to support actionable recommendations.
Journal article. Cancer stem cells (CSCs); a rare, highly adaptable tumour subpopulation.
Mitochondrial dynamics (fission, fusion, biogenesis, mitophagy) and mitochondrial ion signalling form an interconnected regulatory network enabling CSCs to adapt metabolically and signalling states Mitochondrial Ca2+ signalling via MCU, VDACs, and mitochondrial K+ channels regulate membrane potential, OXPHOS, ROS signalling, and bioenergetic adaptation These processes facilitate CSC survival under hypoxia, nutrient deprivation, and anticancer therapy through plasticity and adaptive stress tolerance
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This review identifies mitochondrial dynamics–ion signalling crosstalk as a conceptual framework for understanding CSC therapeutic resistance. However, it does not present clinical evidence or trial data to guide clinical practice; it highlights mechanistic concepts and challenges that require further investigation and validation.
This is a narrative review synthesizing emerging mechanistic concepts about mitochondrial dynamics and ion signalling in cancer stem cells, raising questions about therapeutic targeting rather than reporting original experimental evidence or clinical outcomes.
This review identifies mitochondrial dynamics–ion signalling crosstalk as a conceptual framework for understanding CSC therapeutic resistance. However, it does not present clinical evidence or trial data to guide clinical practice; it highlights mechanistic concepts and challenges that require further investigation and validation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Abstract Cancer stem cells (CSCs) constitute a rare yet highly adaptable tumour subpopulation that drives tumour initiation, intratumorally heterogeneity, metastasis, recurrence, and therapy resistance. Emerging evidence indicates that mitochondrial dynamics and mitochondrial ion signalling form an interconnected regulatory network that enables CSCs to remodel their metabolic and signalling states in response to environmental and therapeutic stress. Mitochondrial architectural remodelling through fission, fusion, biogenesis, and mitophagy cooperates closely with mitochondrial Ca2+ signalling and ion transport systems, including the mitochondrial calcium uniporter (MCU), voltage-dependent anion channels (VDACs), and mitochondrial K+ channels, to regulate mitochondrial membrane potential, oxidative phosphorylation (OXPHOS), reactive oxygen species (ROS) signalling, and bioenergetic adaptation. Selected plasma membrane and ER-associated ion channels further contribute by modulating mitochondrial signalling pathways. Together, these processes govern CSC plasticity, adaptive stress tolerance, and stemness-associated programs, facilitating survival under hypoxia, nutrient deprivation, and anticancer therapy. In this review, we explore how mitochondrial dynamics and ion signalling converge to shape CSC metabolic flexibility and therapeutic resistance. We further discuss emerging diagnostic and therapeutic opportunities targeting mitochondrial dynamics–ion signalling crosstalk, while highlighting key challenges, including CSC heterogeneity, metabolic adaptability, and the need for selective strategies capable of eliminating CSCs while sparing normal stem-cell populations.
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