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Mitochondrial genome acquisition restores respiratory function and tumor-genic potential of cancer cells without mitochondrial DNA.
Tan AS(), Baty JW(), Dong LF(), Bezawork-Geleta A(), Endaya B(), Goodwin J(), Bajzikova M(), Kovarova J(), Peterka M(), Yan B(), Pesdar EA(), Sobol M(), Filimonenko A(), Stuart S(), Vondrusova M(), Kluckova K(), Sachaphibulkij K(), Rohlena J(), Hozak P(), Truksa J(), Eccles D(), Haupt LM(), Griffiths LR(), Neuzil J(), Berridge MV()
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
.
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
.
PMID: 25565207
SENS Approach:
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