Mitochondria break through cellular boundaries (Editorial)

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Author(s)
Neuzil, Jiri
Berridge, Michael V
Griffith University Author(s)
Year published
2019
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In our recent research, we have used respiration-deficient tumour cells to challenge the dogma that mitochondria with their genome are constrained within cells in the body, and to question the concept that mitochondria are primarily the powerhouse of the cell.
Our results have shown that mitochondria move from normal cells in the body to tumour cells without mitochondrial DNA (mtDNA), resulting in respiration recovery and the ability to grow as tumours [1, 2]. Almost a decade earlier, a similar phenomenon had been show in co-cultures of human tumour cells lacking mtDNA with mesenchymal stem cells [3]. The strength of both ...
View more >In our recent research, we have used respiration-deficient tumour cells to challenge the dogma that mitochondria with their genome are constrained within cells in the body, and to question the concept that mitochondria are primarily the powerhouse of the cell. Our results have shown that mitochondria move from normal cells in the body to tumour cells without mitochondrial DNA (mtDNA), resulting in respiration recovery and the ability to grow as tumours [1, 2]. Almost a decade earlier, a similar phenomenon had been show in co-cultures of human tumour cells lacking mtDNA with mesenchymal stem cells [3]. The strength of both of these ground-breaking studies was that they used mtDNA polymorphisms to show repopulation of tumour cells with mtDNA, establishing the origin of mitochondria in the donor cells.
View less >
View more >In our recent research, we have used respiration-deficient tumour cells to challenge the dogma that mitochondria with their genome are constrained within cells in the body, and to question the concept that mitochondria are primarily the powerhouse of the cell. Our results have shown that mitochondria move from normal cells in the body to tumour cells without mitochondrial DNA (mtDNA), resulting in respiration recovery and the ability to grow as tumours [1, 2]. Almost a decade earlier, a similar phenomenon had been show in co-cultures of human tumour cells lacking mtDNA with mesenchymal stem cells [3]. The strength of both of these ground-breaking studies was that they used mtDNA polymorphisms to show repopulation of tumour cells with mtDNA, establishing the origin of mitochondria in the donor cells.
View less >
Journal Title
Aging-US
Volume
11
Issue
13
Copyright Statement
© The Author(s) 2019. This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 Unported (CC BY 3.0) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Subject
Biochemistry and cell biology
Zoology
Oncology and carcinogenesis
Science & Technology
Life Sciences & Biomedicine
Cell Biology
Geriatrics & Gerontology
mitochondrial transfer