High-risk human papillomavirus types 16 and 18 contribute to cervical carcinogenesis through viral oncoproteins that neutralize key cell cycle checkpoints. The primary action of the E6 oncoprotein is:
- A Inhibition of p53 function by sequestration of its transactivation domain
- B Binding of the retinoblastoma protein to free E2F
- C Ubiquitin-mediated proteasomal degradation of p53 ✓
- D Activation of cyclin D-CDK4 complexes
Explanation
HPV E6 recruits a cellular ubiquitin ligase complex containing E6-associated protein so that p53 is tagged with ubiquitin and destroyed by the proteasome, abolishing DNA damage checkpoint control. Option B describes E7, which binds hypophosphorylated RB and releases E2F. Options A and D describe mechanisms used by other oncoproteins, not E6. This E6-p53 and E7-RB pairing is a standard examination favorite.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.