HIV-1 Vpr: enhancing sensitivity of tumors to apoptosis

Curr Drug Deliv. 2004 Oct;1(4):335-44. doi: 10.2174/1567201043334614.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Gene Products, vpr / genetics
  • Gene Products, vpr / physiology*
  • Humans
  • Neoplasms / genetics
  • Neoplasms / physiopathology
  • Neoplasms / therapy*
  • Tumor Suppressor Protein p53 / physiology

Substances

  • Gene Products, vpr
  • Tumor Suppressor Protein p53