Methanol Extract of <i>Commelina</i> Plant Inhibits Oral Cancer Cell Proliferation
Wangta Liu,
Yin-Yin Hsu,
Jen-Yang Tang,
Yuan-Bin Cheng,
Ya-Ting Chuang,
Jiiang-Huei Jeng,
Chia-Hung Yen,
Hsueh-Wei Chang
Affiliations
Wangta Liu
Department of Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Yin-Yin Hsu
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Jen-Yang Tang
School of Post-Baccalaureate Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Yuan-Bin Cheng
Department of Marine Biotechnology and Resources, National Sun Yat-sen University, Kaohsiung 80424, Taiwan
Ya-Ting Chuang
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Jiiang-Huei Jeng
School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Chia-Hung Yen
Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Hsueh-Wei Chang
Department of Biomedical Science and Environmental Biology, PhD Program in Life Science, College of Life Science, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Data regarding the effects of crude extract of Commelina plants in oral cancer treatment are scarce. This present study aimed to assess the proliferation-modulating effects of the Commelina sp. (MECO) methanol extract on oral cancer cells in culture, Ca9-22, and CAL 27. MECO suppressed viability to a greater extent in oral cancer cells than in normal cells. MECO also induced more annexin V, apoptosis, and caspase signaling for caspases 3/8/9 in oral cancer cells. The preferential antiproliferation and apoptosis were associated with cellular and mitochondrial oxidative stress in oral cancer cells. Moreover, MECO also preferentially induced DNA damage in oral cancer cells by elevating γH2AX and 8-hydroxyl-2′-deoxyguanosine. The oxidative stress scavengers N-acetylcysteine or MitoTEMPO reverted these preferential antiproliferation mechanisms. It can be concluded that MECO is a natural product with preferential antiproliferation effects and exhibits an oxidative stress-associated mechanism in oral cancer cells.
