Regulatory Effects of ARV7 on Prostate Specific Antigen
Location
Philadelphia
Start Date
13-5-2015 1:00 PM
Description
Prostate cancer is a common and deadly disease for aging men in the United States. Normal prostate gland function and prostate cancer growth rely on androgen and androgen-receptor (AR) interaction. Binding of androgens leads to AR nuclear translocation. In the nucleus AR regulates its target gene expression through interacting with androgen response elements (ARE) located in the promoter/enhancer regions of the target genes. AR variants form in advanced stages of prostate cancer and some AR variants are hormone independent and possibly beneficial to tumor growth. Previous work has confirmed that a specific AR variant (ARV7) was localized in the nuclei of prostate cancer cells even under androgen-depleted conditions, and is constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. However, the molecular mechanism for ARV7 function in prostate cancer development is not well known. Understanding the mechanisms of ARV7 function in prostate cancer development and strategies against ARV7 should be valuable in combating hormone-independent prostate cancer. PC-3 is an AR negative prostate cancer cell line that we transiently transfected with a plasmid containing AR-V7. RNAs and proteins were purified and used for RT-PCR and Western Blot, respectively. ARV7 protein was successfully expressed when the cells were transfected with the plasmid. One of the AR target genes, prostate specific antigen (PSA), was upregulated in the ARV7 transfected cells compared to the control. We are using this system to explore the repressive effects of different chemicals (resveratrol and metformin) on ARV7 activity
Regulatory Effects of ARV7 on Prostate Specific Antigen
Philadelphia
Prostate cancer is a common and deadly disease for aging men in the United States. Normal prostate gland function and prostate cancer growth rely on androgen and androgen-receptor (AR) interaction. Binding of androgens leads to AR nuclear translocation. In the nucleus AR regulates its target gene expression through interacting with androgen response elements (ARE) located in the promoter/enhancer regions of the target genes. AR variants form in advanced stages of prostate cancer and some AR variants are hormone independent and possibly beneficial to tumor growth. Previous work has confirmed that a specific AR variant (ARV7) was localized in the nuclei of prostate cancer cells even under androgen-depleted conditions, and is constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. However, the molecular mechanism for ARV7 function in prostate cancer development is not well known. Understanding the mechanisms of ARV7 function in prostate cancer development and strategies against ARV7 should be valuable in combating hormone-independent prostate cancer. PC-3 is an AR negative prostate cancer cell line that we transiently transfected with a plasmid containing AR-V7. RNAs and proteins were purified and used for RT-PCR and Western Blot, respectively. ARV7 protein was successfully expressed when the cells were transfected with the plasmid. One of the AR target genes, prostate specific antigen (PSA), was upregulated in the ARV7 transfected cells compared to the control. We are using this system to explore the repressive effects of different chemicals (resveratrol and metformin) on ARV7 activity