Inhibitory Effect of Burmannic Acid for Proliferation and Oxidative Stress Induce Responses of Oral Cancer Cells

The present investigation evaluated the antiproliferation effects of C. burmannii-de-rived BURA on oral cancer cells for the first time. Oral cancer cell lines derived from gin-gival, tongue, and buccal mucosa tissues (Ca9-22, CAL 27, and OC-2) were selected for testing the cellular response to BURA. Oxidative stress in oral disease is related to other systemic diseases in the body such as periodontitis, cardiovascular, pancreatic, gastric, and liver diseases. In the present review, we discuss the various pathways that mediate oxidative cellular damage. In terms of mechanism, BURA per- turbed cell cycle distribution, upregulated mitochondrial superoxide, induced mitochondrial depo- larization, triggered H2AX and 8-hydroxy-2-deoxyguanosine DNA damage, and induced apop- tosis and caspase 3/8/9 activation in oral cancer cells. N-acetylcysteine treatment confirmed oxidative stress as a key factor in promoting antiproliferation, apoptosis, and DNA damage in oral cancer cells. The study demonstrated that BURA generates oxidative stress and causes apoptosis and DNA damage that inhibits oral cancer cell proliferation.