Final answer:
HPV's E7 oncoprotein causes cellular proliferation by inactivating the retinoblastoma protein (Rb), which releases the E2F transcription factors, promoting the cell cycle and cell division. The E6 oncoprotein degrades the tumor suppressor p53, impairing the cell's ability to repair DNA damage or go through apoptosis, allowing mutations to accumulate and cancer to potentially develop.
Step-by-step explanation:
How E7 Induces Cellular Proliferation
The human papillomavirus (HPV) can lead to cervical cancer through the action of viral proteins that alter the normal regulatory mechanisms of the cell cycle. Specifically, HPV encodes for E6 and E7 oncoproteins. While E6 targets the p53 protein, E7 primarily affects another regulatory protein called Rb (retinoblastoma protein). When E7 associates with Rb, it leads to the phosphorylation and inactivation of Rb, freeing the E2F transcription factors. In a healthy cell, E2F is bound and inhibited by Rb, preventing the expression of genes required for DNA synthesis and cellular proliferation. However, when E7 inactivates Rb, E2F is released and can induce the expression of genes that advance the cell cycle, leading to uncontrolled cell division and potentially contributing to the development of cancer.
Regarding p53, E6 facilitates the degradation of this tumor suppressor gene, which under normal conditions acts to prevent cell cycle progression in the case of DNA damage, or initiates apoptosis when damage is irreparable. With p53 neutralized, cells are unable to properly respond to genetic damage, contributing to the accumulation of mutations and the further breakdown of cell cycle regulation.