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

Tan, An S., Baty, James W., Dong, Lan-Feng, Bezawork-Geleta, Ayenachew, Endaya, Berwini, Goodwin, Jacob, Bajzikova, Martina, Kovarova, Jaromira, Peterka, Martin, Yan, Bing, Pesdar, Elham Alizadeh, Sobol, Margarita, Filimonenko, Anatolyj, Stuart, Shani, Vondrusova, Magdalena, Kluckova, Katarina, Sachaphibulkij, Karishma, Rohlena, Jakub, Hozak, Pavel, Truksa, Jaroslav, Eccles, David, Haupt, Larisa M., Griffiths, Lyn R., Neuzil, Jiri and Berridge, Michael V. (2015) Mitochondrial genome acquisition restores respiratory function and tumorigenic potential of cancer cells without mitochondrial DNA. Cell Metabolism, 21 1: 81-94. doi:10.1016/j.cmet.2014.12.003


Author Tan, An S.
Baty, James W.
Dong, Lan-Feng
Bezawork-Geleta, Ayenachew
Endaya, Berwini
Goodwin, Jacob
Bajzikova, Martina
Kovarova, Jaromira
Peterka, Martin
Yan, Bing
Pesdar, Elham Alizadeh
Sobol, Margarita
Filimonenko, Anatolyj
Stuart, Shani
Vondrusova, Magdalena
Kluckova, Katarina
Sachaphibulkij, Karishma
Rohlena, Jakub
Hozak, Pavel
Truksa, Jaroslav
Eccles, David
Haupt, Larisa M.
Griffiths, Lyn R.
Neuzil, Jiri
Berridge, Michael V.
Title Mitochondrial genome acquisition restores respiratory function and tumorigenic potential of cancer cells without mitochondrial DNA
Journal name Cell Metabolism   Check publisher's open access policy
ISSN 1932-7420
1550-4131
Publication date 2015-01-06
Sub-type Article (original research)
DOI 10.1016/j.cmet.2014.12.003
Open Access Status Not yet assessed
Volume 21
Issue 1
Start page 81
End page 94
Total pages 14
Place of publication Cambridge, MA United States
Publisher Cell Press
Language eng
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.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Queensland Brain Institute Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 113 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 114 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Mon, 12 Jun 2017, 10:07:05 EST by Kirstie Asmussen on behalf of Queensland Brain Institute