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Published in: Cancer Cell International 1/2009

Open Access 01-12-2009 | Primary research

The human immunodeficiency virus type 1 Vpr protein and its carboxy-terminally truncated form induce apoptosis in tumor cells

Authors: Mizuho Nonaka, Yoshie Hashimoto, Shin-nosuke Takeshima, Yoko Aida

Published in: Cancer Cell International | Issue 1/2009

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Abstract

The human immunodeficiency virus type 1 (HIV-1) accessory protein Vpr induces apoptosis after cell cycle arrest at the G2 phase in primate cells. We have reported previously that C81, a carboxy-terminally truncated form of Vpr, interferes with cell proliferation and results in apoptosis without G2 arrest. Here, we investigated whether this property of Vpr and C81 could be exploited for use as a potential anticancer agent. First, we demonstrated that C81 induced G1 arrest and apoptosis in all tumor cells tested. In contrast, Vpr resulted in G2 arrest and apoptosis in HeLa and 293 T cells. Vpr also suppressed the damaged-DNA-specific binding protein 1 (DDB1) in HepG2 cells, thereby inducing apoptosis without G2 arrest. G2 arrest was restored when DDB1 was overexpressed in cells that also expressed Vpr. Surprisingly, C81 induced G2 arrest when DDB1 was overexpressed in HepG2 cells, but not in HeLa or 293 T cells. Thus, the induction of Vpr- and C81-mediated cell cycle arrest appears to depend on the cell type, whereas apoptosis was observed in all tumor cells tested. Overall, Vpr and C81 have potential as novel therapeutic agents for treatment of cancer.
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Metadata
Title
The human immunodeficiency virus type 1 Vpr protein and its carboxy-terminally truncated form induce apoptosis in tumor cells
Authors
Mizuho Nonaka
Yoshie Hashimoto
Shin-nosuke Takeshima
Yoko Aida
Publication date
01-12-2009
Publisher
BioMed Central
Published in
Cancer Cell International / Issue 1/2009
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/1475-2867-9-20

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