Please use this identifier to cite or link to this item:
https://doi.org/10.7554/eLife.22187
Title: | Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondrial DNA-deficient cancer cells | Authors: | Dong, L.-F Kovarova, J Bajzikova, M |
Keywords: | mitochondrial DNA red fluorescent protein mitochondrial DNA animal cell Article C57BL/6N mouse cancer cell carcinogenic activity cell respiration chromatin immunoprecipitation confocal microscopy DNA transfer gel electrophoresis heteroplasmy melanoma B16 melanoma cell mitochondrial respiration mouse native blue gel electrophoresis nonhuman oxidative phosphorylation polymerase chain reaction animal C57BL mouse disease model genetics horizontal gene transfer melanoma pathology tumor cell line Animals Cell Line, Tumor Cell Respiration Disease Models, Animal DNA, Mitochondrial Gene Transfer, Horizontal Melanoma Mice, Inbred C57BL |
Issue Date: | 2017 | Citation: | Dong, L.-F, Kovarova, J, Bajzikova, M (2017). Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondrial DNA-deficient cancer cells. eLife 6 : e22187. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.22187 | Rights: | Attribution 4.0 International | Abstract: | Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (r0 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 B16r0 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 B16r0 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. © Dong et al. | Source Title: | eLife | URI: | https://scholarbank.nus.edu.sg/handle/10635/178700 | ISSN: | 2050084X | DOI: | 10.7554/eLife.22187 | Rights: | Attribution 4.0 International |
Appears in Collections: | Elements Staff Publications |
Show full item record
Files in This Item:
File | Description | Size | Format | Access Settings | Version | |
---|---|---|---|---|---|---|
10_7554_eLife_22187.pdf | 6.83 MB | Adobe PDF | OPEN | None | View/Download |
This item is licensed under a Creative Commons License