Figure 5.

Proposed model to illustrate the anticancer activity of surfactin in SCC4 and SCC25 cells. Surfactin reduced the viability of SCC4 and SCC25 cells by induction of apoptosis. Apoptosis promoted by surfactin was associated with activation of caspase and PARP cleavage and was regulated by the mitochondrial pathway, as exemplified by mitochondrial depolarization, cytochrome c release, and down-regulation of the antiapoptotic Bcl-2 protein. Surfactin induced intracellular ROS generation. Intracellular ROS production appeared essential for the activation of the mitochondrial pathway and induction of apoptosis after exposure to surfactin. Oxidative stress due to treatment with surfactin was associated with JNK1/2 activation, as determined by JNK1/2 phosphorylation. After treatment with surfactin, ROS provided a specific environment that resulted in JNK1/2-induced cell death. These findings suggest that surfactin is a potential chemotherapeutic agent for the treatment of oral squamous cell carcinoma.