Haibo Zhang1, Eungyung Kim1, Junkoo Yi2, Huang Hai1, Hyeonjin Kim1, Sijun Park3, Su-Geun Lim3, Si-Yong Kim3, Soyoung Jang3, Kirim Kim4, Eun-Kyong Kim4, Youngkyun Lee5, Zaeyoung Ryoo6, Myoungok Kim7. 1. Department of Animal Science and Biotechnology, ITRD, Kyungpook National University, Sangju, Republic of Korea. 2. Gyeongsangbukdo Livestock Institute Research, Yeongju, Republic of Korea. 3. School of Life Science, Kyungpook National University, Daegu, Republic of Korea. 4. Department of Dental Hygiene, Kyungpook National University, Sangju, Republic of Korea. 5. Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Republic of Korea. 6. School of Life Science, Kyungpook National University, Daegu, Republic of Korea; ok4325@knu.ac.kr jaewoong64@hanmail.net. 7. Department of Animal Science and Biotechnology, ITRD, Kyungpook National University, Sangju, Republic of Korea; ok4325@knu.ac.kr jaewoong64@hanmail.net.
Abstract
BACKGROUND/AIM: [6]-Gingerol, a compound extracted from ginger, has been studied for its therapeutic potential in various types of cancers. However, its effects on oral cancer remain largely unknown. Here, we aimed to investigate the potential anticancer activity and underlying mechanisms of [6]-gingerol in oral cancer cells. MATERIALS AND METHODS: We analyzed the antigrowth effects of [6]-gingerol in oral cancer cell lines by cell proliferation, colony formation, migration, and invasion assays. We detected cell cycle and apoptosis with flow cytometry and further explored the mechanisms of action by immunoblotting. RESULTS: [6]-Gingerol significantly inhibited oral cancer cell growth by inducing apoptosis and cell cycle G2/M phase arrest. [6]-Gingerol also inhibited oral cancer cell migration and invasion by up-regulating E-cadherin and down-regulating N-cadherin and vimentin. Moreover, [6]-gingerol induced the activation of AMPK and suppressed the AKT/mTOR signaling pathway in YD10B and Ca9-22 cells. CONCLUSION: [6]-Gingerol exerts anticancer activity by activating AMPK and suppressing the AKT/mTOR signaling pathway in oral cancer cells. Our findings highlight the potential of [6]-gingerol as a therapeutic drug for oral cancer treatment.
BACKGROUND/AIM: [6]-Gingerol, a compound extracted from ginger, has been studied for its therapeutic potential in various types of cancers. However, its effects on oral cancer remain largely unknown. Here, we aimed to investigate the potential anticancer activity and underlying mechanisms of [6]-gingerol in oral cancer cells. MATERIALS AND METHODS: We analyzed the antigrowth effects of [6]-gingerol in oral cancer cell lines by cell proliferation, colony formation, migration, and invasion assays. We detected cell cycle and apoptosis with flow cytometry and further explored the mechanisms of action by immunoblotting. RESULTS: [6]-Gingerol significantly inhibited oral cancer cell growth by inducing apoptosis and cell cycle G2/M phase arrest. [6]-Gingerol also inhibited oral cancer cell migration and invasion by up-regulating E-cadherin and down-regulating N-cadherin and vimentin. Moreover, [6]-gingerol induced the activation of AMPK and suppressed the AKT/mTOR signaling pathway in YD10B and Ca9-22 cells. CONCLUSION: [6]-Gingerol exerts anticancer activity by activating AMPK and suppressing the AKT/mTOR signaling pathway in oral cancer cells. Our findings highlight the potential of [6]-gingerol as a therapeutic drug for oral cancer treatment.