Functional effects of cancer mitochondria on energy metabolism and tumorigenesis: utility of transmitochondrial cybrids.
Reprogramming of energy metabolism is one of the hallmarks of cancer. In normal conditions, cells rely on mitochondrial oxidative phosphorylation to provide energy for cellular activities. Cancer cells are characterized by increased glycolysis and reduced mitochondrial respiratory function. In the past decade, somatic mitochondrial DNA alterations are found to be common in all types of cancers. However, the functional significance of the altered cancer mitochondria is largely unknown. This is because the bulk of cancer properties are regulated by nuclear encoded genes. To overcome this problem, the transmitochondrial cybrid system, which allows the study of the effect of cancer mitochondria in a common nuclear background, has been used. Here we review the accumulating evidence that altered cancer mitochondria affect the respiratory chain function and oncogenic properties in vitro and in vivo using cybrid technologies.
Kaipparettu
Benny Abraham
BA
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA.
Ma
Yewei
Y
Wong
Lee-Jun C
LJ
D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D004272:DNA, Mitochondrial / Q000378:metabolism*; D004734:Energy Metabolism; D017353:Gene Deletion; D015972:Gene Expression Regulation, Neoplastic; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism*; D012306:Risk
D004272:DNA, Mitochondrial