Although it has been established that persistent infection with high risk human papillomavirus (HR-HPV) is the main cause in the development of cervical cancer, the HR-HPV infection is also related with the cause of a significant fraction of other human malignancies from the mucosal squamous epithelial such as anus, vagina, vulva, penis and oropharynx. HR-HPV infection induces cell proliferation, cell death evasion and genomic instability resulting in cell transformation, due to HPV proteins, which target and modify the function of differents cell molecules and organelles, such as mitochondria. Mitochondria are essential in the production of the cellular energy by oxidative phosphorylation (OXPHOS), in the metabolism of nucleotides, aminoacids (aa), and fatty acids, even in the regulation of cell death processes such as apoptosis or mitophagy. Thus, mitochondria have a significant role in the HPV-related cancer development. This review focuses on the role of HPV and mitochondria in HPV-related cancer development, and treatments associated to mitochondrial apoptosis.
Keywords: HPV-related cancer; High risk human papillomavirus (HR-HPV); mitochondria; mitochondria metabolism; mitochondrial apoptosis; oxidative stress (OS); reactive oxygen species (ROS).
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