CHED 838 |
| The role of the Vitamin D Receptor (VDR) protein and 1-α,25-dihydroxycholecalciferol [1,25 (OH)2-D3]is one that is of significant importance in the study of mammary tissue tumorigenesis. Previous research has examined the preventative and therapeutic effects of VDR and 1,25 (OH)2-D3 against breast cancer. Current VDR research models include transgenic VDR knockout mice, Human Mammary Epithelial (HME) cell lines and human breast cancer cell lines. In previous studies, VDR Knockout mice have proven to be problematic due to their need to be on a special calcium diet and adverse skin and hair deformities that interfere with the study of the role of VDR in mammary tissue. A transgenic mouse model that localizes the knockout of the VDR gene to the mammary tissue would eliminate these problems. This was achieved through the MMTV-Cre/LoxP Recombination System and a qPCR assay from the mammary, hepatic and renal tissue that showed the tissue specific knockout was localized to the mammary gland with a functional VDR still found in the renal and hepatic tissue. The effects of 1,25 D3 and an apoptotic inducing agent, Etoposide, on normal human mammary epithelial cells were performed to determine the possibility of crosstalk between VDR and p53. Western Blotting and qPCR determined the effects on gene expression and protein levels of p53, p21 and VDR at various time points. T47D breast cancer cells were stably transfected with a vector that caused the knockdown of the expression of 1α-hydroxylase, the enzyme responsible for attaching the 2nd hydroxyl group to Vitamin D3 converting it to its active form that binds to VDR. A total of five stable transfected T47D cell lines were generated. Future studies will investigate the effects of knocking down 1α-hydroxylase in these breast cancer cells. |
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Undergraduate Research Poster Session: Biochemistry
2:00 PM-4:00 PM, Monday, April 7, 2008 Morial Convention Center -- Hall A, Poster
Division of Chemical Education |