HIV-1 Vpr: Enhancing Sensitivity of Tumors to Apoptosis

Title: HIV-1 Vpr: Enhancing Sensitivity of Tumors to Apoptosis

Volume: 1 Issue: 4

Author(s): Karuppiah Muthumani, Andrew Y. Choo, Daniel S. Hwang, Kenneth E. Ugen and David B. Weiner

Affiliation:

Keywords: hiv-1, vpr, nf-kappab, p53, mitochondria, cancer, caspase and apoptosis

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 Vprs 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.

Cite this article as:

Muthumani Karuppiah, Choo Y. Andrew, Hwang S. Daniel, Ugen E. Kenneth and Weiner B. David, HIV-1 Vpr: Enhancing Sensitivity of Tumors to Apoptosis, Current Drug Delivery 2004; 1 (4) . https://dx.doi.org/10.2174/1567201043334614