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Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondrial DNA-deficient cancer cells
LF. Dong, J. Kovarova, M. Bajzikova, A. Bezawork-Geleta, D. Svec, B. Endaya, K. Sachaphibulkij, AR. Coelho, N. Sebkova, A. Ruzickova, AS. Tan, K. Kluckova, K. Judasova, K. Zamecnikova, Z. Rychtarcikova, V. Gopalan, L. Andera, M. Sobol, B. Yan, B....
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2013
Free Medical Journals
od 2012
PubMed Central
od 2012
Europe PubMed Central
od 2012
ProQuest Central
od 2012-01-01
Open Access Digital Library
od 2012-01-01
Open Access Digital Library
od 2013-01-01
Health & Medicine (ProQuest)
od 2012-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2012
PubMed
28195532
DOI
10.7554/elife.22187
Knihovny.cz E-zdroje
- MeSH
- buněčné dýchání MeSH
- melanom patologie MeSH
- mitochondriální DNA genetika MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední C57BL MeSH
- nádorové buněčné linie MeSH
- přenos genů horizontální * MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (ρ0cells) is linked to the acquisition of the host mtDNA. However, the mechanism of mtDNA movement between cells remains unresolved. To determine whether the transfer of mtDNA involves whole mitochondria, we injected B16ρ0mouse melanoma cells into syngeneic C57BL/6Nsu9-DsRed2mice that express red fluorescent protein in their mitochondria. We document that mtDNA is acquired by transfer of whole mitochondria from the host animal, leading to normalisation of mitochondrial respiration. Additionally, knockdown of key mitochondrial complex I (NDUFV1) and complex II (SDHC) subunits by shRNA in B16ρ0cells abolished or significantly retarded their ability to form tumours. Collectively, these results show that intact mitochondria with their mtDNA payload are transferred in the developing tumour, and provide functional evidence for an essential role of oxidative phosphorylation in cancer.
CNC Center for Neuroscience and Cell Biology University of Coimbra Cantanhede Portugal
CSIR Institute of Genomics and Integrative Biology New Delhi India
Department of Zoology Faculty of Science Charles University Prague Czech Republic
Institute of Biotechnology Czech Academy of Sciences Prague Czech Republic
Institute of Molecular Genetics Czech Academy of Sciences Prague Czech Republic
Malaghan Institute of Medical Research Wellington New Zealand
School of Medical Science Griffith University Southport Australia
Citace poskytuje Crossref.org
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