Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondrial DNA-deficient cancer cells
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- Lan-Feng Dong
- School of Medical Science, Griffith University, Southport, Australia
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- Jaromira Kovarova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Martina Bajzikova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Ayenachew Bezawork-Geleta
- School of Medical Science, Griffith University, Southport, Australia
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- David Svec
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Berwini Endaya
- School of Medical Science, Griffith University, Southport, Australia
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- Karishma Sachaphibulkij
- School of Medical Science, Griffith University, Southport, Australia
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- Ana R Coelho
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Natasa Sebkova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Anna Ruzickova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- An S Tan
- Malaghan Institute of Medical Research, Wellington, New Zealand
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- Katarina Kluckova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Kristyna Judasova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Katerina Zamecnikova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Zuzana Rychtarcikova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Vinod Gopalan
- School of Medical Science, Griffith University, Southport, Australia
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- Ladislav Andera
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Margarita Sobol
- Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
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- Bing Yan
- School of Medical Science, Griffith University, Southport, Australia
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- Bijay Pattnaik
- CSIR Institute of Genomics and Integrative Biology, New Delhi, India
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- Naveen Bhatraju
- CSIR Institute of Genomics and Integrative Biology, New Delhi, India
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- Jaroslav Truksa
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Pavel Stopka
- Department of Zoology, Faculty of Science, Charles University, Prague, Czech Republic
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- Pavel Hozak
- Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
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- Alfred K Lam
- School of Medicine, Griffith University, Southport, Australia
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- Radislav Sedlacek
- Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
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- Paulo J Oliveira
- CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Cantanhede, Portugal
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- Mikael Kubista
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Anurag Agrawal
- CSIR Institute of Genomics and Integrative Biology, New Delhi, India
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- Katerina Dvorakova-Hortova
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Jakub Rohlena
- Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic
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- Michael V Berridge
- Malaghan Institute of Medical Research, Wellington, New Zealand
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- Jiri Neuzil
- School of Medical Science, Griffith University, Southport, Australia
抄録
<jats:p>Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (ρ0 cells) 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 B16ρ0 mouse melanoma cells into syngeneic C57BL/6Nsu9-DsRed2 mice 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 B16ρ0 cells 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.</jats:p>
収録刊行物
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- eLife
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eLife 6 e22187-, 2017-02-15
eLife Sciences Publications, Ltd