RT Journal Article SR Electronic 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 FD International Institute of Anticancer Research SP 3193 OP 3201 DO 10.21873/invivo.12614 VO 35 IS 6 A1 HAIBO ZHANG A1 EUNGYUNG KIM A1 JUNKOO YI A1 HUANG HAI A1 HYEONJIN KIM A1 SIJUN PARK A1 SU-GEUN LIM A1 SI-YONG KIM A1 SOYOUNG JANG A1 KIRIM KIM A1 EUN-KYONG KIM A1 YOUNGKYUN LEE A1 ZAEYOUNG RYOO A1 MYOUNGOK KIM YR 2021 UL http://iv.iiarjournals.org/content/35/6/3193.abstract AB 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.