癌症与衰老中的 DNA 损伤与线粒体
DNA damage and mitochondria in cancer and aging.
机构信息
Laboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD, USA.
出版信息
Carcinogenesis. 2020 Dec 31;41(12):1625-1634. doi: 10.1093/carcin/bgaa114.
Age and DNA repair deficiencies are strong risk factors for developing cancer. This is reflected in the comorbidity of cancer with premature aging diseases associated with DNA damage repair deficiencies. Recent research has suggested that DNA damage accumulation, telomere dysfunction and the accompanying mitochondrial dysfunction exacerbate the aging process and may increase the risk of cancer development. Thus, an area of interest in both cancer and aging research is the elucidation of the dynamic crosstalk between the nucleus and the mitochondria. In this review, we discuss current research on aging and cancer with specific focus on the role of mitochondrial dysfunction in cancer and aging as well as how nuclear to mitochondrial DNA damage signaling may be a driving factor in the increased cancer incidence with aging. We suggest that therapeutic interventions aimed at the induction of autophagy and mediation of nuclear to mitochondrial signaling may provide a mechanism for healthier aging and reduced tumorigenesis.
年龄和 DNA 修复缺陷是癌症发展的强危险因素。这反映在癌症与与 DNA 损伤修复缺陷相关的早衰疾病的合并症中。最近的研究表明，DNA 损伤的积累、端粒功能障碍和随之而来的线粒体功能障碍会加剧衰老过程，并可能增加癌症发展的风险。因此，癌症和衰老研究的一个关注领域是阐明细胞核和线粒体之间的动态串扰。在这篇综述中，我们讨论了衰老和癌症的当前研究，特别关注线粒体功能障碍在癌症和衰老中的作用，以及核到线粒体 DNA 损伤信号转导如何成为衰老时癌症发病率增加的驱动因素。我们认为，旨在诱导自噬和介导核到线粒体信号转导的治疗干预可能为更健康的衰老和减少肿瘤发生提供一种机制。
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