Files
Abstract
Current therapeutic options for melanoma patients are limited by the ability of melanocytes to withstand higher levels of DNA damage compared to other cells. A genome-wide microarray was performed to unmask a more targeted approach to melanoma cancer therapy, which identified microRNA-122 (miR-122) as highly expressed in melanoma cells. Previous studies linked lysophosphatidic acid receptor-3 (LPAR3) expression to melanoma cell viability. Therefore, we hypothesized that not only is miR-122 regulated by LPAR3, but is also mediating cell viability by activating an oncogenic signaling pathway. Our data supports the conclusion that the upregulation and export of miR-122 out of the cell is a response to LPAR3 overexpression. Our work is the first study to illustrate a role for miR-122 in melanoma. In addition, our work shows that miR-122 targets the β-catenin oncogenic pathway and facilities its localization to the nucleus. Future studies on miR-122’s agonistic contributions to melanoma cell viability and proliferation may lead to a more targeted approach for patients. Preliminary data suggests a role for the LPAR3-miR-122 axis in the evolution of melanocytes to melanoma.