Dibenzoylmethane (DBM) is a minor constituent of licorice root, a common ingredient in many sunscreens, and a known neoplasia inhibitor. Although DBM has exhibited anti-neoplastic activity in many studies, no reports offer definitive mechanisms of action for DBM on tumor growth inhibition. Our laboratory was the first to report the antineoplastic effects of DBM in prostate cancer cells. Understanding changes in human prostate cancer cells’ extracellular matrix (ECM) protein composition when treated with DBM may represent a potential target for antitumor therapy. Preliminary data shows that beta-actin, an important protein involved in adhesion, was decreased in a dose-dependent manner when LNCaP human prostate cancer cells were treated with 50 uM DBM and assessed by western blotting. In this study, we seek to explain why tumors are more vulnerable to drug therapies after being treated with the natural agent DBM by examining changes in the levels of important adhesion proteins. Using the CHEMICON® ECM Cell Adhesion Array, the tumor microenvironment and important specific cell surface integrins, monitoring in vitro cell differentiation, or screening potential cell adhesion promoters/inhibitors were further assessed. These data suggest that cancer cell vulnerability may be linked with the physical properties of the ECM.
