Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses.
Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses.
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DOI：
10.1007/s11515-014-1332-0
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发表时间：
2014-12
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中科院分区：
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15%-20%的人类癌症与致癌病毒感染有关。致癌病毒包括HPV、乙肝病毒、丙型肝炎病毒和HTLV-1，它们以线粒体为靶标，影响细胞的增殖和存活。致癌病毒基因产物还可触发活性氧的产生，从而导致DNA氧化损伤，增强致癌宿主信号通路。病毒癌基因还可能颠覆线粒体质量控制机制，如吞丝分裂和代谢适应途径，以促进病毒复制。在这里，我们将综述病毒对有丝分裂和代谢适应的调节及其在病毒肿瘤发生中的作用的最新进展。
Between 15–20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.