The E6 oncoprotein of high-risk HPV strains promotes cervical carcinogenesis primarily by:
- A Inactivating Rb by hyperphosphorylation
- B Activating RAS signaling through GTP loading
- C Binding and degrading p53 via ubiquitin-mediated proteolysis ✓
- D Upregulating survivin expression
Explanation
HPV E6 oncoprotein binds the cellular E6-AP ubiquitin ligase to form a complex that ubiquitinates p53, targeting it for proteasomal degradation. This eliminates p53-mediated cell-cycle arrest and apoptosis, allowing genomic instability to accumulate. HPV E7 — not E6 — targets Rb by displacing the E2F transcription factor from the Rb-E2F complex. RAS activation and survivin upregulation are not direct E6 mechanisms.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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