In cervical intraepithelial neoplasia (CIN), the E6 oncoprotein of high-risk HPV (types 16/18) promotes carcinogenesis primarily by:

• A Inactivating RB by phosphorylation
• B Activating the PI3K/AKT/mTOR survival pathway
• C Upregulating telomerase reverse transcriptase directly
• D Binding and degrading p53 via ubiquitin-proteasome pathway ✓

Explanation

High-risk HPV E6 oncoprotein binds to p53 tumour suppressor protein and targets it for ubiquitin-mediated proteasomal degradation via the E6-AP ubiquitin ligase, effectively inactivating the DNA damage checkpoint and apoptotic response. The complementary HPV E7 protein binds and inactivates the RB family proteins by displacing E2F transcription factors, driving cells into S-phase. Together, E6 (anti-p53) and E7 (anti-RB) work synergistically to abrogate the two major tumour suppressor pathways, enabling neoplastic transformation of cervical epithelium.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.