A heteroplasmic, not homoplasmic, mitochondrial DNA mutation promotes tumorigenesis via alteration in reactive oxygen species generation and apoptosis

• Published in: Human molecular genetics Vol. 18; no. 9; pp. 1578 - 1589
• Main Authors: Park, Jeong Soon, Sharma, Lokendra Kumar, Li, Hongzhi, Xiang, Ruihua, Holstein, Deborah, Wu, Jun, Lechleiter, James, Naylor, Susan L., Deng, Janice J., Lu, Jianxin, Bai, Yidong
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.05.2009; Oxford Publishing Limited (England)
• Subjects: Ageing, cell death; Animals; Apoptosis; Biological and medical sciences; Cell Line, Tumor; Cell physiology; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes; Cell Transformation, Neoplastic; DNA, Mitochondrial - genetics; DNA, Mitochondrial - metabolism; Electron Transport Complex I - genetics; Electron Transport Complex I - metabolism; Fundamental and applied biological sciences. Psychology; Genetics of eukaryotes. Biological and molecular evolution; Humans; Male; Mice; Mice, Nude; Mitochondria - genetics; Mitochondria - metabolism; Mitochondrial Proteins - genetics; Mitochondrial Proteins - metabolism; Molecular and cellular biology; Mutation; NADH Dehydrogenase - genetics; NADH Dehydrogenase - metabolism; Neoplasms - genetics; Neoplasms - metabolism; Neoplasms - physiopathology; Reactive Oxygen Species - metabolism; Reactive oxygen species; Alteration; Genetics; Mitochondrial DNA; Mutation; Carcinogenesis; Apoptosis

Mitochondrial alteration has been long proposed to play a major role in tumorigenesis. Recently, mitochondrial DNA (mtDNA) mutations have been found in a variety of cancer cells. In this study, we examined the contribution of mtDNA mutation and mitochondrial dysfunction in tumorigenesis first using...