Presentation Type
Poster
Growth attenuation of murine B16.F10 melanoma tumors mediated by an HIV protein, Vpr (viral protein R)
Abstract
Because of the highly metastatic nature of melanoma tumors, there exists a necessity for the characterization of novel chemotherapeutic drugs effective against metastatic disease. The HIV-1 viral protein R (Vpr) has been demonstrated to induce cell cycle arrest and apoptosis in rapidly proliferating cells, such as tumor cells. This characteristic makes Vpr a viable candidate as a novel anti-tumor agent. Furthermore, previous investigations have determined that the carboxy terminal region of Vpr (i.e. amino acids 65-83) induces significant cell apoptosis. This report demonstrates that B16.F10 melanoma cells treated with a peptide encompassing the C-terminal region showed significant subcutaneous tumor attenuation when injected into syngeneic C57BL6 mice. Tumor volume analysis revealed an inhibition of tumor growth, which had been previously associated with the induction of cell apoptosis. Specifically, treatment with a peptide containing the carboxy terminal region of Vpr resulted in greater than 90% inhibition of melanoma tumor growth 15 days after tumor injection. Novel delivery methods for Vpr are needed to enhance its cytotoxicity in order to achieve complete regression of melanoma tumors.
This study was supported, in part, by a pilot grant from the Florida Center of Excellence on Biomolecular Identification and Targeted Therapeutics (FCoEBitt) to Kenneth Ugen.
Categories
Biomedical Sciences
Research Type
Research Assistant
Mentor Information
Dr. Kenneth E. Ugen
Growth attenuation of murine B16.F10 melanoma tumors mediated by an HIV protein, Vpr (viral protein R)
Because of the highly metastatic nature of melanoma tumors, there exists a necessity for the characterization of novel chemotherapeutic drugs effective against metastatic disease. The HIV-1 viral protein R (Vpr) has been demonstrated to induce cell cycle arrest and apoptosis in rapidly proliferating cells, such as tumor cells. This characteristic makes Vpr a viable candidate as a novel anti-tumor agent. Furthermore, previous investigations have determined that the carboxy terminal region of Vpr (i.e. amino acids 65-83) induces significant cell apoptosis. This report demonstrates that B16.F10 melanoma cells treated with a peptide encompassing the C-terminal region showed significant subcutaneous tumor attenuation when injected into syngeneic C57BL6 mice. Tumor volume analysis revealed an inhibition of tumor growth, which had been previously associated with the induction of cell apoptosis. Specifically, treatment with a peptide containing the carboxy terminal region of Vpr resulted in greater than 90% inhibition of melanoma tumor growth 15 days after tumor injection. Novel delivery methods for Vpr are needed to enhance its cytotoxicity in order to achieve complete regression of melanoma tumors.
This study was supported, in part, by a pilot grant from the Florida Center of Excellence on Biomolecular Identification and Targeted Therapeutics (FCoEBitt) to Kenneth Ugen.
