There is recent evidence that suggests that cancer development and progression may be influenced by an interplay between cancer cells and the surrounding tumor microenvironment, which includes extracellular matrix (ECM) components. Understanding changes in human prostate cancer cell progression and ECM protein composition, as well as the overall cytoskeleton when treated with novel therapeutic agents, may represent a potential mechanism for antitumor therapy. Dibenzoylmethane (DBM) is a minor constituent of licorice root, a common ingredient in many sunscreens, and a known neoplasia inhibitor. Our laboratory was the first to report the antineoplastic effects of DBM in prostate cancer cells. Preliminary data shows that β−actin, an important protein involved in adhesion, was decreased in a dose-dependent manner when LNCaP human prostate cancer cells were treated with 50 μM DBM and assessed by western blotting. In this study, we seek to explain why prostate 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. LNCaP cells were treated with 50 μM DBM for 72 hours, and changes in adhesion protein expression were assessed by a chromogenic activity assay. These data suggest that DBM may disrupt ECM homeostasis and cancer cell vulnerability may be linked to the physical properties of the ECM with deregulation of collagen I, fibronectin, laminin, and tenascin by DBM.
