Gallic acid (GA) has long been associated with a wide range of biological activities. In this study, its antitumoreffect against B16F10 melanoma cells was demonstrated by MTT assay, cell migration assay, wound-healing assay, and flowcytometric analysis. GA with a concentration >200 μM shows apoptotic activity toward B16F10 cells. According to Westernblotting data, overexpressions of cleaved forms of caspase-9, caspase-3, and PARP-1 and pro-apoptotic Bax and Bad, accompaniedby underexpressed anti-apoptotic Bcl-2 and Bcl-xL indicate that GA induces B16F10 cell apoptosis via mitochondrial pathway.The 2-DE based comparative proteomics was further employed in B16F10 cells with and without GA treatment for a large-scaleprotein expression profiling. A total of 41 differential protein spots were quantified, and their identities were characterized usingLC-MS/MS analysis and database matching. In addition to some regulated proteins that were associated with apoptosis,interestingly, some identified proteins involved in glycolysis such as glucokinase, α-enolase, aldolase, pyruvate kinase, andGAPDH were simultaneously up-regulated, which reveals that the GA-induced cellular apoptosis in B16 melanoma cells isassociated with metabolic glycolysis.
