Title

Inhibitory Effects of Vitamin D3 on Rad51 in MCF-7 Cells

Poster Number

23

Format

Poster Presentation

Abstract/Artist Statement

Breast Cancer is the second most common form of cancer in women. Rad51 is a protein that participates in homologous recombination of DNA during double stranded break repair and has been shown to interact with the breast cancer proteins, BRCA1 and BRCA2. Vitamin-D3 (VD3) inhibits cell proliferation and initiates cell death, apoptosis, in some cancer cell lines. We are investigating whether VD3 inhibits Rad51 in MCF-7 line, a breast cancer cell line. MCF-7 cells were grown and harvested for western blots, and were used to spot on slides for microarray analysis. The Bradford assay was used to determine protein concentration in various cell lysates. It was found that MCF-7 lysates were positive for the Rad51 protein using both western blot and microarray techniques. Next, MCF-7 cells were treated with VD3 or an ethanol control and harvested during specific time points, generating a time course for VD3 treatment. Previous work in the Albala lab has shown that VD3 does inhibit the growth of head and neck cancer cells. We aim to demonstrate this in the MCF-7 cell line. Ongoing experiments will include comparisons of western blots with microarrays using the MCF-7 lysates after the time course of treatment with VD3. If VD3 inhibits Rad51 and DNA repair, then this may reveal a mechanism for the increased cell death in those cancer cells treated with VD3.

Location

DeRosa University Center, Ballroom B

Start Date

1-5-2010 1:00 PM

End Date

1-5-2010 3:00 PM

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May 1st, 1:00 PM May 1st, 3:00 PM

Inhibitory Effects of Vitamin D3 on Rad51 in MCF-7 Cells

DeRosa University Center, Ballroom B

Breast Cancer is the second most common form of cancer in women. Rad51 is a protein that participates in homologous recombination of DNA during double stranded break repair and has been shown to interact with the breast cancer proteins, BRCA1 and BRCA2. Vitamin-D3 (VD3) inhibits cell proliferation and initiates cell death, apoptosis, in some cancer cell lines. We are investigating whether VD3 inhibits Rad51 in MCF-7 line, a breast cancer cell line. MCF-7 cells were grown and harvested for western blots, and were used to spot on slides for microarray analysis. The Bradford assay was used to determine protein concentration in various cell lysates. It was found that MCF-7 lysates were positive for the Rad51 protein using both western blot and microarray techniques. Next, MCF-7 cells were treated with VD3 or an ethanol control and harvested during specific time points, generating a time course for VD3 treatment. Previous work in the Albala lab has shown that VD3 does inhibit the growth of head and neck cancer cells. We aim to demonstrate this in the MCF-7 cell line. Ongoing experiments will include comparisons of western blots with microarrays using the MCF-7 lysates after the time course of treatment with VD3. If VD3 inhibits Rad51 and DNA repair, then this may reveal a mechanism for the increased cell death in those cancer cells treated with VD3.