MDA-MB-231 exposed to Melatonin shows increase in beta-catenin expression and no increase in E-cadherin expression

E-cadherin plays an essential role in cell-cell connections. Loss of these connections is an important step in the transition of normal cells into cancer cells. The epithelial-mesenchymal transition (EMT) is the transition from a normal cell phenotype to metastatic cells that can grow without restrictions and invade other tissues. Loss of E-cadherin expression is a marker for EMT. Melatonin has been shown to increase E-cadherin expression in MCF7 breast cancer cells. MDA-MB-231 cells are metastatic prostate cancer cells that no longer express E-cadherin or in low concentrations. MDA-MB-231 cells were exposed to melatonin to see if melatonin can restore and increase E-cadherin expression and, therefore, reverse the EMT process and return the cells to a more epithelial phenotype. MDA-MB-231 was exposed continuously to melatonin for 3 weeks at 3nM, 3µM, and 3mM concentrations. After 7 days, exposed cells were split and prepared for immunofluorescence staining and Western blotting. Melatonin toxicity was determined by MTT assay. Results show that E-cadherin protein levels increased in a time and concentration dependent trend at the 3nM and 3mM concentrations; 3mM proved to be toxic to the cells and caused cell death. In addition, the number of cells that expressed E-cadherin increased, with the greatest expression being found at the intercellular connections. This suggests that functional E-cadherin is present. These results may be significant in treatment by reversing metastatic tumor development. Future experiments will involve patient derived and metastatic breast cancer cell lines.