Open Access
REVIEW
The Effect of Oncogene Proteins of Human Papillomaviruses on Apoptosis Pathways in Prostate Cancer
1
Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
2
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
3
Department of Microbiology, Faculty of Medical Sciences, Islamic Azad University, Kazerun, Iran
4
Drug Applied Research Centre, Tabriz University of Medical Sciences, Tabriz, Iran
5
Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
6
Student Research Committee, Iran University of Medical Sciences, Tehran, Iran
7
Department of Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
* Corresponding Authors: Hossein Bannazadeh Baghi. Emails: ;
Oncologie 2022, 24(2), 227-245. https://doi.org/10.32604/oncologie.2022.020648
Received 05 December 2021; Accepted 28 March 2022; Issue published 29 June 2022
Abstract
The ability of host cells to activate apoptosis is perhaps the most potent weapon for helping cells eliminate viruses. Human papillomaviruses (HPV) activate several pathways, enabling the infected cells to avoid extrinsic and intrinsic apoptosis pathways. The incapacity of prostatic epithelial cells to induce apoptosis leads to the invasive development of prostate cancer. For the pathogenesis of prostate cancer, several risk factors have been reported; for example, some viruses and infectious diseases have been proposed as causative agents for their relation to prostate diseases. According to several studies, high-risk human papillomaviruses cause malignancy by interfering with the apoptotic and inflammatory pathways; these viruses, such as HPV16 and HPV18, block apoptotic pathways and result in prostate cancer. This review is dedicated to presenting a summary of oncogenes (E5, E6, and E7) HR-HPVs’ functions on signaling pathways, inflammation in prostate tumorigenesis, and emphasizing the link between these oncogenes with apoptosis and prostate cancer.Keywords
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