期刊
AGEING RESEARCH REVIEWS
卷 9, 期 -, 页码 S47-S58出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2010.08.009
关键词
Aging; Cancer; Mitochondria; mtDNA; Somatic mutation
资金
- Taipei Veterans General Hospital [V99E2-008]
- National Science Council [NSC96-2320-B-010-006, NSC97-2320-B-010-022-MY3, NSC98-3111-B-010-005]
- Center of Excellence for Cancer Research at Taipei Veterans General Hospital
- Department of Health [DOH99-TD-C-111-007]
- Executive Yuan, Taiwan, Republic of China
- Ministry of Education. Aim for the Top University Plan, Taiwan
Mitochondria are intracellular organelles responsible for generating ATP through respiration and oxidative phosphorylation (OXPHOS), producing reactive oxygen species, and initiating and executing apoptosis. Mitochondrial dysfunction has been observed to be an important hallmark of aging and cancer. Because mitochondrial DNA (mtDNA) is important in maintaining functionally competent organelles, accumulation of mtDNA mutations can affect energy production, oxidative stress, and cell survival, which may contribute to aging and/or carcinogenesis. This review outlines a variety of somatic mtDNA mutations identified in aging tissues and human cancers, as well as recent advances in understanding the causal role of mtDNA mutations in the aging process and cancer progression. Mitochondrial dysfunction elicited by somatic mutations in mtDNA could induce apoptosis in aging cells and some cancer cells with severe mtDNA mutations. In addition, it could activate mitochondria-to-nucleus retrograde signaling to modulate the expression of nuclear genes involved in a metabolic shift from OXPHOS to glycolysis, facilitate cells to adapt to altered environments and develop resistance to chemotherapeutic agents, or promote metastatic properties of cancer cells. These findings suggest that accumulation of somatic mtDNA mutations is not only an important contributor to human aging but also plays a critical role in cancer progression. (C) 2010 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据