@Article{biocell.2025.059787,
AUTHOR = {Sahel Abyar, Shahrzad Shoraka, Seyed Masoud Hosseini, Mohammad Reza Zali, Seyed Reza Mohebbi},
TITLE = {A Review of Mitochondrial Involvement in Cell Death Pathways Induced by Oncogenic Viruses},
JOURNAL = {BIOCELL},
VOLUME = {49},
YEAR = {2025},
NUMBER = {2},
PAGES = {221--251},
URL = {http://www.techscience.com/biocell/v49n2/59699},
ISSN = {1667-5746},
ABSTRACT = {Oncogenic viruses include both DNA and RNA viruses which contribute to cancer development by disrupting cellular regulation and interfering in the immune responses. These viruses do not directly cause cancer but instead integrate their genetic material into the host genome thus, affecting cell cycle and tumor suppression. This deregulation also leads to impaired immune function and promotes tumor progression by disrupting the removal of infected cells. Generally, innate immunity consists of two important members, including mitochondria and cell deaths, which impact each other as well. Due to the close correlation between viruses, cell death pathways (apoptosis, necroptosis, and pyroptosis), and mitochondria (mitochondrial antiviral-signaling protein and reactive oxygen species generation), targeting these immune system representatives may offer therapeutic strategies to control the progression of oncogenic viral infections. Some previous studies have covered the association of oncogenic viruses with mitochondria and cell death pathways, respectively, but mitochondria and cell death interact with each other, separately, and this interaction may play a role in the progression of cancer induced by oncogenic viruses. Hence, the purpose of this review is to discuss the relationship between cell death, mitochondria, and viral oncogenesis, focusing on the most surveyed oncogenic viruses’ mechanisms of action.},
DOI = {10.32604/biocell.2025.059787}
}