CAV VP3 Apoptin selectively induces G2/M arrest and apoptosis in human cancer cells without affecting normal primary cells. Apoptin engages in nucleocytoplasmic shuttling in cancer cells and normal primary cells; post arrest it is observed that in infected cancer cells Apoptin localizes to the nucleus, whereas Apoptin is observed in the cytoplasm of normal primary cells. We have attempted to uncouple multimerization from nuclear export to determine if both are required to induce apoptosis in cancer cells. Elimination of nuclear export and diminished multimerization of Apoptin is sufficient to induce apoptosis. Further research in this area will need to be conducted in order to determine if synthesis of a small molecule therapeutic will be able to duplicate the functionality of Apoptin.
Worcester Polytechnic Institute
Major Qualifying Project
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Chemistry and Biochemistry