TY - JOUR T1 - [6]-Gingerol Suppresses Oral Cancer Cell Growth by Inducing the Activation of AMPK and Suppressing the AKT/mTOR Signaling Pathway JF - In Vivo JO - In Vivo SP - 3193 LP - 3201 DO - 10.21873/invivo.12614 VL - 35 IS - 6 AU - HAIBO ZHANG AU - EUNGYUNG KIM AU - JUNKOO YI AU - HUANG HAI AU - HYEONJIN KIM AU - SIJUN PARK AU - SU-GEUN LIM AU - SI-YONG KIM AU - SOYOUNG JANG AU - KIRIM KIM AU - EUN-KYONG KIM AU - YOUNGKYUN LEE AU - ZAEYOUNG RYOO AU - MYOUNGOK KIM Y1 - 2021/11/01 UR - http://iv.iiarjournals.org/content/35/6/3193.abstract N2 - 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. ER -