[Cell cycle G2 arrest, cell death and nuclear localization induced by human immunodeficiency virus type 1 protein R (VPR) in cervical cancer cells].
OBJECTIVE
To explore the possibility of using Vpr as a biological agent for anticancer therapy.


METHODS
A HIV-1 wild type Vpr and a mutant VprX gene were expressed and tested in a cervical cancer HeLa cell line. The ability of Vpr to induce cell cycle G2 arrest and cell death was measured by flow cytometric analysis. Nuclear localization of Vpr was visualized by fluorescent light emitted from the green fluorescent protein (GFP) -Vpr fusion protein.


RESULTS
Consistent with early reports, Vpr, not VprX, induced G2 arrest. However, both Vpr and VprX were able to induce cell death in HeLa cells. We also demonstrated that the nuclear localization of Vpr could be determined by using a GFP-Vpr fusion protein.


CONCLUSIONS
This is the first report documenting in mammalian cells that G2 arrest and cell death induced by Vpr are two independent functions. The unique biological properties of Vpr shown in cervical cancer cells suggest that Vpr may be a useful biological agent for anti -cancer therapy.
Yang
J
J
Children' s Memorial Institute for Education and Research, USA.
Yi
Y
Y
Wang
J
J
D016923:Cell Death / Q000235:genetics; D005260:Female; D016195:G2 Phase / Q000235:genetics*; D015870:Gene Expression; D016336:Gene Products, vpr / Q000096:biosynthesis; D016334:Genes, vpr; D015497:HIV-1 / Q000235:genetics*; D006367:HeLa Cells; D006801:Humans; D014162:Transfection; D054325:vpr Gene Products, Human Immunodeficiency Virus
D016336:Gene Products, vpr; D054325:vpr Gene Products, Human Immunodeficiency Virus