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

Authors

  • Su-Ling Liu Experimental Forest College of Bioresources and Agriculture, National Taiwan University, Zhushan Township, Nantou County-55750, Taiwan.
  • Kun-Han Yang Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.
  • Che-Wei Yang Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.
  • Min-Yu Lee Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.
  • Ya-Ting Chuang Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.
  • Yan-Ning Chen Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.
  • Chung-Yi Chen School of Medical and Health Sciences, Fooyin University, Kaohsiung-83102, Taiwan.

DOI:

https://doi.org/10.9734/bpi/namms/v3/18990D

Keywords:

Burmannic acid, spices, oral cancer, DNA damage, apoptosis, oxidative stress

Abstract

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 \(\gamma\)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.

Published

2023-06-01

How to Cite

Su-Ling Liu, Kun-Han Yang, Che-Wei Yang, Min-Yu Lee, Ya-Ting Chuang, Yan-Ning Chen, & Chung-Yi Chen. (2023). Inhibitory Effect of Burmannic Acid for Proliferation and Oxidative Stress Induce Responses of Oral Cancer Cells. New Advances in Medicine and Medical Science Vol. 3, 101–121. https://doi.org/10.9734/bpi/namms/v3/18990D

Issue

New Advances in Medicine and Medical Science Vol. 3

Section

Chapters