Cited by 785Mitochondrial Function and PathologyCancer, Hypoxia, and MetabolismCancer and biochemical research

Mitochondrial genome acquisition restores respiratory function and tumorigenic potential of cancer cells without mitochondrial DNA

Open access
Tan, An S., Baty, James W., Dong, Lan-Feng, Bezawork-Geleta, Ayenachew, Endaya, Berwini, Goodwin, Jacob, Bajzikova, Martina, Kovarova, Jaromira +17 more·2015·Cell Metabolism

Abstract

We report that tumor cells without mitochondrial DNA (mtDNA) show delayed tumor growth, and that tumor formation is associated with acquisition of mtDNA from host cells. This leads to partial recovery of mitochondrial function in cells derived from primary tumors grown from cells without mtDNA and a shorter lag in tumor growth. Cell lines from circulating tumor cells showed further recovery of mitochondrial respiration and an intermediate lag to tumor growth, while cells from lung metastases exhibited full restoration of respiratory function and no lag in tumor growth. Stepwise assembly of mitochondrial respiratory (super)complexes was correlated with acquisition of respiratory function. Our findings indicate horizontal transfer of mtDNA from host cells in the tumor microenvironment to tumor cells with compromised respiratory function to re-establish respiration and tumor-initiating efficacy. These results suggest pathophysiological processes for overcoming mtDNA damage and support the notion of high plasticity of malignant cells.

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Crossref · 10.1016/j.cmet.2014.12.003

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  • Targeted depletion of mitochondrial DNA reduces the tumorigenic potential of cancer cell lines in vitro and in vivo.

    “targeted depletion of mitochondrial DNA reduces the tumorigenic potential of cancer cell lines in vitro and in vivo”

    From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Tan et al., 2015

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Authors
Tan, A. S., Baty, J. W., Dong, L.-F., Bezawork-Geleta, A., Endaya, B., Goodwin, J., Bajzikova, M., Kovarova, J., Peterka, M., Yan, B., Pesdar, E. A., Sobol, M., Filimonenko, A., Stuart, S., Vondrusova, M., Kluckova, K., Sachaphibulkij, K., Rohlena, J., Hozak, P., Truksa, J., Eccles, D., Haupt, L. M., Griffiths, L. R., Neuzil, J., & Berridge, M. V.
Affiliations
  • Malaghan Institute of Medical Research (NZ)
  • Griffith University (AU)
  • Czech Academy of Sciences (CZ)
  • Queensland University of Technology (AU)
Corresponding author
Berridge, Michael V.
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2015-01
Volume
21
Issue
1
Pages
81-94
ISSN
1550-4131 (ISSN-L)
OpenAlex
W2030637794
Cited by
785
References
64
Citations by year
2026: 60 · 2025: 60 · 2024: 65 · 2023: 73 · 2022: 70 · 2021: 63 · 2020: 92 · 2019: 73 · 2018: 62 · 2017: 62 · 2016: 68 · 2015: 35 · 2014: 1
FWCI
32.66
Type
journal article
Language
en
Open access
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • ASEP (publishedVersion)
  • QUT ePrints (Queensland University of Technology) (acceptedVersion)
  • Griffith Research Online (submittedVersion)
Funders
  • Breast Cancer Research Trust
  • Cancer Society of New Zealand
  • Grantová Agentura České Republiky
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
Keywords
tumor microenvironment, mitochondrial respiration, circulating tumor cells, lung metastasis, cancer stem cells, mitochondrial DNA damage, tumor plasticity
MeSH terms
Animals, Citrate (si)-Synthase, DNA, Mitochondrial, Energy Metabolism, Lung Neoplasms, Melanoma, Experimental, Mice, Inbred BALB C, Mice, Inbred C57BL, Mitochondria, NADH Dehydrogenase, RNA, Messenger, Transplantation, Homologous, Mice, SCID, Mice, Inbred NOD, Reactive Oxygen Species, Electron Transport Chain Complex Proteins, Cell Line, Tumor, Cell Proliferation, Mice

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