Fig. 1
From: Emerging paradigms: unmasking the role of oxidative stress in HPV-induced carcinogenesis
Various processes are involved in HPV-mediated carcinogenesis and the impact of oncoproteins on oxidative stress [21, 22, 52, 53]. In HPV-mediated carcinogenesis, integration of HPV DNA into the host leads to the disruption of E1 and E2 reading frames, resulting in overexpression of E6 and E7 oncogenes. E6 inhibits tumor suppressor protein (p53) and pro-apoptotic protein (BAK), preventing apoptosis and facilitating viral DNA replication. E6 also targets PDZ proteins, enhancing transformative capabilities. E7 interacts with the tumor suppressor (pRb), promoting carcinogenesis by disrupting cell cycle regulation. E7 facilitates E2F-induced transcription by releasing E2F from pRb-E2F complexes, increasing CDK2 activity and centrosome amplification. E7's CD3 domain interacts with proteins like p21 and p27, suppressing their activity and allowing cells to bypass DNA damage-induced cell cycle arrest. These mechanisms collectively create an environment conducive to viral DNA replication and malignant cell transformation [18, 20,21,22,23, 25, 26, 28, 54]