Resveratrol attenuates endogenous <i>BST2</i> expression and disrupts downstream functional effects in high grade breast cancer cells.

<p><b><i>A.</i></b> Tumor cells (CCdl54) treated with resveratrol for 24 hrs displayed a significant decline in <i>BST2</i> expression denoted by asterisks (p<0.01). QPCR analysis performed in triplicate, and normalized to <i>ACTB</i> expression. <b><i>B.</i></b> Enhancement of apoptotic cell death induced by 24 hr tamoxifen treatment of 6-day resveratrol (20 µM) supplemented tumor cultures plated in Matrigel. <b><i>Top panel</i></b> – immunolocalization of cleaved caspase 3 (green) in apoptotic cells; nuclei counterstained with PI (red). Bar - 25 µm. <b><i>Bottom panel</i></b> – Immunostaining data plotted as apoptotic index represents proportion of PI-stained nuclei (>100) vs. immunopositive cells in multiple microscopic fields scanned with a 20× objective, and averaged. Asterisk denotes significant (p<0.01) differences in the apoptotic index in the presence of tamoxifen alone vs. resveratrol pretreatment followed by tamoxifen. <b><i>C.</i></b> Resveratrol-mediated suppression of the cell cycle in high grade tumor cells (CCdl54, CCdl672) is similar to the effects of <i>BST2</i> silencing. A statistically significant reduction in S-phase resulting from both approaches for <i>BST2</i> attenuation is accompanied by an increase in the G1-fraction in independent cell lines. The data derived from BrdU labeling of 2 independent cell lines represents an average of 2 separate FACS runs on each cell line, with each treatment performed in triplicate sets. <b><i>D.</i></b> Induction of <i>AP2</i> expression in high grade tumor cells (CCdl675, CCdl54) treated with increasing concentrations of resveratrol. QPCR analysis performed in triplicate, and normalized to <i>ACTB</i> expression. Asterisks indicate significant differences (p<0.01) between control and treated samples.