Inhibition of Monoacylglycerol Lipase Suppresses Lipopolysaccharide-Enhanced Melanoma Proliferation and Migration

Background/Objectives: Lipid metabolism dysregulation contributes to cancer progression. Monoacylglycerol lipase (MAGL) breaks down 2-arachidonoylglycerol (2-AG) into glycerol and arachidonic acid, a substrate for cyclooxygenase-2 (COX-2) to produce pro-inflammatory mediators such as prostaglandin E2 (PGE2). Lipopolysaccharide (LPS) activation of Toll-like receptor 4 (TLR4) triggers inflammatory pathways, including COX-2/PGE2 signaling, implicated in diseases such as melanoma. MAGL inhibition reduces prostaglandins and other inflammatory mediators, but its role in inflammation-driven melanoma progression remains unexplored. This study investigated how JZL184, a selective MAGL inhibitor, and 2-AG affect LPS-induced inflammation, proliferation, and migration in B16 melanoma cells.