Journal
CELL METABOLISM
Volume 21, Issue 1, Pages 81-94Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2014.12.003
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Funding
- Genesis Oncology Trust
- Cancer Society of New Zealand
- Breast Cancer Research Trust
- National Health and Medical Research Council
- Cancer Council Queensland
- Clem Jones Foundation
- Czech Science Foundation [P301/10/1937, GA15-02203S, P305/12/1708, P301/12/1851]
- Australian Research Council
- Technology Agency of the Czech Republic [TE01020118]
- Ministry of Industry and Trade of the Czech Republic [FR-TI3/588]
- Griffith University
- Australian Government EIF Super Science Funds, Therapeutic Innovation Australia Queensland Node project
- BIOCEV European Regional Development Fund [CZ.1.05/1.1.00/02.0109]
- Malaghan Institute
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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 reestablish 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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