- A mutant version of E2F-1, called truncated E2F (E2Ftr), is more effective at causing cancer cell death (apoptosis) than the normal E2F-1, but the exact mechanisms behind this are not completely understood.
- The study found that the pro-apoptotic protein Harakiri (Hrk) is significantly increased in melanoma cells when either E2F-1 or E2Ftr is overexpressed, and this up-regulation does not rely on the traditional p53 pathway.
- Additionally, another factor called DREAM appears to play a role in this apoptosis process, as its levels rise with E2F-1 and E2Ftr overexpression;