About: Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA     Goto   Sponge   NotDistinct   Permalink

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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 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.
  • 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. (en)
Title
  • Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA
  • Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA (en)
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  • Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA
  • Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA (en)
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  • RIV/86652036:_____/15:00440852!RIV15-GA0-86652036
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  • I, P(ED1.1.00/02.0109), P(GAP301/10/1937), P(GAP301/12/1851), P(GAP305/12/1708)
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  • 281
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  • RIV/86652036:_____/15:00440852
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  • ELECTRON-TRANSPORT CHAIN; MAMMALIAN MITOCHONDRIA; TUNNELING NANOTUBES (en)
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  • US - Spojené státy americké
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  • [7B6265780D37]
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  • Cell Metabolism
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  • 21
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  • Hozák, Pavel
  • Neužil, Jiří
  • Rohlena, Jakub
  • Sobol, Margaryta
  • Dong, L. F.
  • Truksa, Jaroslav
  • Goodwin, J.
  • Klučková, Katarína
  • Eccles, D.
  • Vondrusová, Magdaléna
  • Bezawork-Geleta, A.
  • Peterka, Martin
  • Bajziková, Martina
  • Kovářová, Jaromíra
  • Filimonenko, Anatolij
  • Alizadeh Pesdar, E.
  • Berridge, M. V.
  • Endaya, B.
  • Griffiths, L. R.
  • Haupt, D.
  • Sachaphibulkij, K.
  • Stuart, S.
  • Tan, A. S.
  • Yan, B.
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  • 000347467900012
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  • 1550-4131
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  • 10.1016/j.cmet.2014.12.003
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