The oncogenic mechanism by which HPV E6 protein drives carcinogenesis in cervical epithelium is most accurately described as:
- A E6 binds E6AP (E6-associated protein), an E3 ubiquitin ligase, targeting p53 for proteasomal degradation ✓
- B E6 directly mutates the KRAS proto-oncogene, activating MAP kinase proliferation signals
- C E6 binds and inactivates Rb (retinoblastoma protein), releasing E2F transcription factors
- D E6 inhibits telomerase, promoting chromosomal instability and malignant transformation
Explanation
HPV E6 oncoprotein exerts its carcinogenic effect by binding E6AP (UBE3A), a cellular E3 ubiquitin ligase, forming a complex that ubiquitinates p53 and directs it to the 26S proteasome for degradation. Loss of p53 tumor suppressor function prevents cell cycle arrest and apoptosis in response to DNA damage. E7 (not E6) binds and inactivates Rb. E6 also activates telomerase (hTERT), enabling cellular immortalization, and this is another E6 function — but Rb inactivation is specifically E7's role.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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Written and medically reviewed by the StethoPrep medical team.