HIV-1 Vpr: enhancing sensitivity of tumors to apoptosis.
Cancers can adapt several evasive functions including apoptosis evasion, self-sufficiency in growth signals, insensitivity to anti-growth signals, sustained angiogenesis, limitless replication potential, tissue invasion and metastasis. The invariable hurdle for development of therapies against such aberrant conditions requires both selective and potent cytotoxicity. Analysis of HIV-1 Vpr's apoptotic and anti-proliferative activity have revealed potentially important implications for cancer therapy. Accordingly, we have reviewed the properties of Vpr that will likely contribute to its efficacious function as an anti-tumor agent. Among these are its ability to induce cell cycle arrest, inhibit inflammation, provoke p53 independent apoptosis, and selective killing of rapidly dividing cells.
Muthumani
Karuppiah
K
Dept. of Pathology and Lab. Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Choo
Andrew Y
AY
Hwang
Daniel S
DS
Ugen
Kenneth E
KE
Weiner
David B
DB
D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D016336:Gene Products, vpr / Q000235:genetics / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000503:physiopathology / Q000628:therapy*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D016336:Gene Products, vpr; D016159:Tumor Suppressor Protein p53