Mitochondrial dynamics in cancer

  • Unique Paper ID: 185824
  • PageNo: 2923-2936
  • Abstract:
  • Mitochondria are key players in cellular homeostasis, not just as major ATP production site but also as regulators of apoptosis, metabolic signalling, and innate immunity. One of their characteristic elements is the ability to dynamically change shape, size, and distribution by way of two stringently controlled processes: mitochondrial fission (division) and fusion (merging). Both are referred to collectively as mitochondrial dynamics and are vital to preserving mitochondrial function and cellular integrity. In cancer, this dynamic balance is commonly disrupted. Tumour cells tend to have increased mitochondrial fission, leading to fragmented mitochondria that are conducive to fast proliferation, apoptosis resistance, and enhanced metastatic ability. Suppression of fusion, on the other hand, inhibits mitochondrial repair and enhances oxidative stress, thereby enhancing malignancy. Moreover, mitophagy (exclusive breakdown of defective mitochondria) and biogenesis (production of new mitochondria) mechanisms of mitochondrial quality control are frequently usurped by cancer cells to cope with both metabolic and therapeutics stress. Considering the key role played by mitochondrial dynamics in the pathophysiology of cancer, these activities offer strong candidate targets for new therapeutic interventions. Pharmacological inhibition of excessive fission—e.g., by DRP1 inhibitors—or improvement of fusion by upregulation of proteins such as mitofusin-2 (MFN2), has been effective in preclinical models. Disrupting mitochondrial homeostasis in cancer cells by these manipulations may inhibit tumour growth, sensitize malignant cells to standard therapies, and eventually lead to improved patient outcomes. Greater insights into mitochondrial dynamics and their control within the tumour microenvironment would open avenues for development of more targeted and effective therapies against cancer.

Copyright & License

Copyright © 2026 Authors retain the copyright of this article. This article is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

BibTeX

@article{185824,
        author = {Pallavi Ingle and Kalpana Dabhade and Yatindra Mathur},
        title = {Mitochondrial dynamics in cancer},
        journal = {International Journal of Innovative Research in Technology},
        year = {2025},
        volume = {12},
        number = {5},
        pages = {2923-2936},
        issn = {2349-6002},
        url = {https://ijirt.org/article?manuscript=185824},
        abstract = {Mitochondria are key players in cellular homeostasis, not just as major ATP production site but also as regulators of apoptosis, metabolic signalling, and innate immunity. One of their characteristic elements is the ability to dynamically change shape, size, and distribution by way of two stringently controlled processes: mitochondrial fission (division) and fusion (merging). Both are referred to collectively as mitochondrial dynamics and are vital to preserving mitochondrial function and cellular integrity. In cancer, this dynamic balance is commonly disrupted. Tumour cells tend to have increased mitochondrial fission, leading to fragmented mitochondria that are conducive to fast proliferation, apoptosis resistance, and enhanced metastatic ability. Suppression of fusion, on the other hand, inhibits mitochondrial repair and enhances oxidative stress, thereby enhancing malignancy. Moreover, mitophagy (exclusive breakdown of defective mitochondria) and biogenesis (production of new mitochondria) mechanisms of mitochondrial quality control are frequently usurped by cancer cells to cope with both metabolic and therapeutics stress. Considering the key role played by mitochondrial dynamics in the pathophysiology of cancer, these activities offer strong candidate targets for new therapeutic interventions.  
Pharmacological inhibition of excessive fission—e.g., by DRP1 inhibitors—or improvement of fusion by upregulation of proteins such as mitofusin-2 (MFN2), has been effective in preclinical models. Disrupting mitochondrial homeostasis in cancer cells by these manipulations may inhibit tumour growth, sensitize malignant cells to standard therapies, and eventually lead to improved patient outcomes. Greater insights into mitochondrial dynamics and their control within the tumour microenvironment would open avenues for development of more targeted and effective therapies against cancer.},
        keywords = {Mitochondrial fission, Mitochondrial dynamics, Mitochondrial fusion, Mitochondrial biogenesis, Mitophagy,},
        month = {October},
        }

Cite This Article

Ingle, P., & Dabhade, K., & Mathur, Y. (2025). Mitochondrial dynamics in cancer. International Journal of Innovative Research in Technology (IJIRT), 12(5), 2923–2936.

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