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Human papillomavirus E6 and E7 oncoproteins are viral proteins encoded by high-risk HPV types, especially HPV 16 and HPV 18. They are essential for malignant transformation, acting by interfering with host cell cycle and apoptosis regulation. E6 degrades tumor suppressor p53, inhibiting apoptosis and promoting genomic instability. E7 binds and promotes degradation of the retinoblastoma protein (pRb), unleashing E2F transcriptional activity and driving cell cycle progression. These proteins are required for both initiation and maintenance of HPV-induced cancers and serve as key biomarkers and therapeutic targets in HPV-related disease. Therapeutic approaches focus on inhibiting their production or activity through vaccines, RNA targeting strategies, and gene editing. Detection of E6/E7 is increasingly used for screening for cervical and anogenital pre-cancer and cancer.
Blockade or degradation of E6/E7 transcripts or proteins. Restoration of p53 (by inhibiting E6). Restoration of pRb (by inhibiting E7). Induction of apoptosis and senescence by loss of viral oncogene function.
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