Vitamin D3 Inhibits RAD51 in Human Breast Cancer
Poster Number
1
Format
Poster Presentation
Faculty Mentor Name
Joana Albala
Faculty Mentor Department
Biological Sciences
Abstract/Artist Statement
Breast Cancer is the second most common form of cancer in women. We are investigating the role of Vitamin D on the DNA repair protein, Rad51, in a breast cancer cell line, MCF7. Rad51 is a protein that participates in repair of DNA double-strand breaks and impairment in Rad51 function in some types breast cancer may be part of the initiation of the disease. The active form of vitamin D, Vitamin-D3 (VD3), inhibits cell proliferation and initiates cell death or apoptosis. My research examined the effect of VD3 on the expression of Rad51 in the MCF7 cell line. MCF7 cells were cultured, treated with VD3, and harvested. Analysis of Rad51 expression was performed by Western blot analysis using several Rad51- specific antibodies. In addition, I have used a cell-based array to perform cell culture in a miniaturized format. By this technique, multiple treatments may be applied to a several cell populations, in parallel, in a cost and time efficient manner. The preliminary conclusion is that treatment with VD3 does inhibit the growth of MCF7 cells. More importantly, this works shows that VD3 decreases the expression of Rad51, which may in turn lead to cell death if repair of DNA double-strand breaks is reduced. These results are similar to what our lab has found in a head and neck cancer cell line. Future experiments will examine whether there is reduced DNA repair capacity of Rad51 and increased apoptosis that may be important to induce cell death in breast cancer cells.
Location
DeRosa University Center, Ballroom
Start Date
21-4-2011 6:00 PM
End Date
21-4-2011 8:00 PM
Vitamin D3 Inhibits RAD51 in Human Breast Cancer
DeRosa University Center, Ballroom
Breast Cancer is the second most common form of cancer in women. We are investigating the role of Vitamin D on the DNA repair protein, Rad51, in a breast cancer cell line, MCF7. Rad51 is a protein that participates in repair of DNA double-strand breaks and impairment in Rad51 function in some types breast cancer may be part of the initiation of the disease. The active form of vitamin D, Vitamin-D3 (VD3), inhibits cell proliferation and initiates cell death or apoptosis. My research examined the effect of VD3 on the expression of Rad51 in the MCF7 cell line. MCF7 cells were cultured, treated with VD3, and harvested. Analysis of Rad51 expression was performed by Western blot analysis using several Rad51- specific antibodies. In addition, I have used a cell-based array to perform cell culture in a miniaturized format. By this technique, multiple treatments may be applied to a several cell populations, in parallel, in a cost and time efficient manner. The preliminary conclusion is that treatment with VD3 does inhibit the growth of MCF7 cells. More importantly, this works shows that VD3 decreases the expression of Rad51, which may in turn lead to cell death if repair of DNA double-strand breaks is reduced. These results are similar to what our lab has found in a head and neck cancer cell line. Future experiments will examine whether there is reduced DNA repair capacity of Rad51 and increased apoptosis that may be important to induce cell death in breast cancer cells.