Magnolia: Effects on Breast Cancer Cells
Sir Winston Churchill
Floor Location : S 195 H
Breast cancer is one of the most prevalent cancers among women. Although the prognosis for localized tumours is very good, there is still a need for effective treatments for metastatic breast cancer. Natural product extracts have been successfully developed as therapeutic agents for several human diseases including cancer. One example is the synthetic derivatives of taxol (e.g, Paclitaxel), originally extracted from the bark of the Pacific yew tree (Taxus brevifolia). Paclitaxel is currently a chemotherapeutic treatment option indicated in some forms of metastatic breast cancer. The major extracts of Magnolia officinalis tree bark, honokiol and magnolol, have been shown to induce apoptosis in some human cancer cell lines. However, little research has been done to determine the efficacy of honokiol and magnolol in limiting the growth of human breast cancer cells. Using the human breast cancer cell lines, MDA MB-231 and MCF-7, we determined if these Magnolia bark extracts inhibited cell growth and also discovered the optimal in vitro drug concentration. To assess cell growth in the presence of these drugs we used several complementary assays including: manual viable cell counts with a hemocytometer, mitochondrial activity MTS assay and an Annexin V apoptosis assay. Using the manual viability counting method, honokiol was the most effective compound, completely inhibiting cell growth and killing all MDA MB-231 cells at 40 M. Magnolol displayed the same effect at 100 M. Similar results were obtained using MCF-7 cells. The MTS assay suggested that both drugs affected cell viability at concentrations of more than 80 M but the assay was potentially unreliable for drug concentrations of 30 - 60 M (a possible technical artifact). In the Annexin V apoptosis assay, after 24 hours of exposure to a low concentration of honokiol or magnolol (10 M), 3% of the honokiol treated cells began to show signs of apoptosis (annexin V-positive) compared to untreated cells. There was not a significant difference between the magnolol treated cells and the control at this concentration and time frame. Our work has effectively enhanced our understanding of magnolol and honokiol as anti-carcinogenic agents and suggests further investigation of their therapeutic potential is warranted.