Cell cycle arrest and apoptosis
The HIV-1 accessory gene vpr encodes a conserved 96-amino acid protein that is necessary and sufficient for the HIV-1-induced block of cellular proliferation and induction of apoptosis. Expression of vpr in CD4 + lymphocytes results in G2 arrest, followed by apoptosis. ATR, as a cellular factor that mediates Vpr-induced cell cycle arrest, is required for activation of the Breast Cancer-Associated Protein-1 (BRCA1). In addition, the Growth Arrest and DNA Damage protein (GADD45) is upregulated by Vpr in an ATR-dependent manner. Posttranscriptional silencing of either ATR or GADD45 leads to nearly complete suppression of the pro-apoptotic and/or cell cycle arrest effect of Vpr.
1. A method of inducing apoptosis in a cancer cell, the method comprising:
introducing HIV-1 Viral protein R (Vpr) and Breast Cancer-Associated Protein I (BRCA1) to a cancer cell; and
inducing apoptosis in the cancer cell; wherein the cancer cell has been identified as lacking a functional BRCA1 gene.
2. The method according to claim 1 , wherein the cancer cell is in a subject.
3. The method according to claim 2 , wherein the subject is a mammal.
4. The method according to claim 1 , wherein the cancer cell comprises a cell culture system.
5. A method of treating a cancer in a subject comprising conducting on the subject the method of claim 2 .
6. The method of claim 5 , wherein the cancer is breast cancer.
7. The method of claim 1 , wherein the Vpr and BRCA1 are expressed by an expression vector.