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Peer-reviewedCC BYEMBO Reports

Mitotic assembly of respiratory supercomplexes ensures accurate cell division and fuels tumor growth

  • Ting Wang1
  • Aoxing Cheng2
  • Lingyu Kong2
  • Weiyi You2
  • Jihua Liu2
  • Xing Liu3
  • Xuebiao Yao3
  • Yi Yang4
  • Yuzheng Zhao4
  • Weiwei Yang5
  • Kaiguang Zhang1
  • Zhenye Yang1
1 more authors
  • Jing Guo1
5 affiliations
  1. 1Department of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China
  2. 2State Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China
  3. 3Ministry of Education Key Laboratory for Membraneless Organelles and Cellular Dynamics, University of Science and Technology of China
  4. 4Optogenetics & Synthetic Biology Interdisciplinary Research Center, State Key Laboratory of Bioreactor Engineering, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology
  5. 5Key Laboratory of Multi-cell Systems, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences
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Abstract

As cells progress from interphase into mitosis, fluctuating metabolic demands coincide with mitochondrial fission. However, the mechanisms by which mitochondria coordinate morphological changes and metabolic adjustments during mitosis remain poorly understood. Using proteomic analysis of BN-PAGE fractions, we show that assembly of the mitochondrial respiratory supercomplexes, comprising electron transport chain complexes I, III, and IV, is markedly enhanced during mitosis in HeLa and MDA-MB-468 cancer cells. Mechanistically, the upregulation of specific CI subunits, including NDUFA3, drives the modular assembly of supercomplexes in mitosis. We further demonstrate that CDK1 promotes the translation of NDUFA3 to enable supercomplex formation. Disruption of this process impairs mitochondrial integrity, energy production, and redox homeostasis, leading to ROS accumulation that triggers mitotic cell death and chromosome segregation defects across multiple models. Importantly, inhibiting mitotic supercomplex assembly induces chromosome mis‑segregation and suppresses tumor growth in vivo. Our findings reveal supercomplex assembly as a key mechanism coordinating mitochondrial fission with metabolic adaptation to support cell division and tumor proliferation in these cancer cell contexts.

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Cite

BibTeXRIS
BibTeX
@article{wang2026mitotic,
  title = {{Mitotic assembly of respiratory supercomplexes ensures accurate cell division and fuels tumor growth}},
  author = {Ting Wang and Aoxing Cheng and Lingyu Kong and Weiyi You and Jihua Liu and Xing Liu and Xuebiao Yao and Yi Yang and Yuzheng Zhao and Weiwei Yang and Kaiguang Zhang and Zhenye Yang and Jing Guo},
  journal = {EMBO Reports},
  year = {2026},
  month = sep,
  doi = {10.1038/s44319-026-00937-8},
  url = {https://doi.org/10.1038/s44319-026-00937-8},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Mitotic assembly of respiratory supercomplexes ensures accurate cell division and fuels tumor growth
AU  - Ting Wang
AU  - Aoxing Cheng
AU  - Lingyu Kong
AU  - Weiyi You
AU  - Jihua Liu
AU  - Xing Liu
AU  - Xuebiao Yao
AU  - Yi Yang
AU  - Yuzheng Zhao
AU  - Weiwei Yang
AU  - Kaiguang Zhang
AU  - Zhenye Yang
AU  - Jing Guo
PY  - 2026
DA  - 2026/09/01
JO  - EMBO Reports
DO  - 10.1038/s44319-026-00937-8
UR  - https://doi.org/10.1038/s44319-026-00937-8
AB  - As cells progress from interphase into mitosis, fluctuating metabolic demands coincide with mitochondrial fission. However, the mechanisms by which mitochondria coordinate morphological changes and metabolic adjustments during mitosis remain poorly understood. Using proteomic analysis of BN-PAGE fractions, we show that assembly of the mitochondrial respiratory supercomplexes, comprising electron transport chain complexes I, III, and IV, is markedly enhanced during mitosis in HeLa and MDA-MB-468 cancer cells. Mechanistically, the upregulation of specific CI subunits, including NDUFA3, drives the modular assembly of supercomplexes in mitosis. We further demonstrate that CDK1 promotes the translation of NDUFA3 to enable supercomplex formation. Disruption of this process impairs mitochondrial integrity, energy production, and redox homeostasis, leading to ROS accumulation that triggers mitotic cell death and chromosome segregation defects across multiple models. Importantly, inhibiting mitotic supercomplex assembly induces chromosome mis‑segregation and suppresses tumor growth in vivo. Our findings reveal supercomplex assembly as a key mechanism coordinating mitochondrial fission with metabolic adaptation to support cell division and tumor proliferation in these cancer cell contexts.
SN  - 1469-3178
ER  -