Abstract
Aging is a major risk factor for developing cancer, suggesting that these two events may represent two sides of the same coin. It is becoming clear that some mechanisms involved in the aging process are shared with tumorigenesis, through convergent or divergent pathways. Increasing evidence supports a role for mitochondrial dysfunction in promoting aging and in supporting tumorigenesis and cancer progression to a metastatic phenotype. Here, a summary of the current knowledge of three aspects of mitochondrial biology that link mitochondria to aging and cancer is presented. In particular, the focus is on mutations and changes in content of the mitochondrial genome, activation of mitochondria-to-nucleus signaling and the newly discovered mitochondria-telomere communication.
Highlights
Mitochondria are cellular organelles that play a pivotal role in maintaining cellular homeostasis by regulating energy metabolism, cell survival and proliferation
This review provides an overview of the convergent and divergent roles that mitochondrial dysfunction may play in cellular processes linked to aging and cancer, with a specific focus on mitochondrial DNA, mitochondria-to-nucleus signaling and telomere shortening
Subsequent studies have shown that these antiretroviral drugs have mitochondria as off-target sites, and in particular, they inhibit polymerase γ (POLγ), causing mtDNA mutations and depletion that result in mitochondrial dysfunction [47]
Summary
Mitochondria are cellular organelles that play a pivotal role in maintaining cellular homeostasis by regulating energy metabolism, cell survival and proliferation. Mitochondrial dysfunction leading to changes in nuclear gene expression may affect the risk of degenerative diseases, cancer and aging [7,8,9,10]. At first glance, aging and cancer may seem to be two opposite processes, the first implying a slow decline of cellular and organismal functions, the second providing fitness to the cells. In reality, these two processes are strictly interconnected and share common origins. This review provides an overview of the convergent and divergent roles that mitochondrial dysfunction may play in cellular processes linked to aging and cancer, with a specific focus on mitochondrial DNA, mitochondria-to-nucleus signaling and telomere shortening
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