Department of Animal Science and Biotechnology, ITRD, Kyungpook National University, Sangju, Republic of Korea.
Gyeongsangbukdo Livestock Institute Research, Yeongju, Republic of Korea.
In Vivo. 2021 Nov-Dec;35(6):3193-3201. doi: 10.21873/invivo.12614.
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.
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.
[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.
[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.
背景/目的：[6]-姜酚是从生姜中提取的一种化合物，其在各种类型癌症中的治疗潜力已得到研究。然而，其对口腔癌的作用仍知之甚少。在这里，我们旨在研究[6]-姜酚在口腔癌细胞中的潜在抗癌活性及其作用机制。
我们通过细胞增殖、集落形成、迁移和侵袭实验分析[6]-姜酚对口腔癌细胞系的生长抑制作用。我们通过流式细胞术检测细胞周期和细胞凋亡，并通过免疫印迹进一步探讨其作用机制。
[6]-姜酚通过诱导细胞凋亡和细胞周期 G2/M 期阻滞显著抑制口腔癌细胞生长。[6]-姜酚还通过上调 E-钙黏蛋白和下调 N-钙黏蛋白和波形蛋白来抑制口腔癌细胞的迁移和侵袭。此外，[6]-姜酚在 YD10B 和 Ca9-22 细胞中诱导 AMPK 的激活，并抑制 AKT/mTOR 信号通路。
[6]-姜酚通过激活 AMPK 和抑制 AKT/mTOR 信号通路在口腔癌细胞中发挥抗癌活性。我们的研究结果强调了[6]-姜酚作为口腔癌治疗的治疗药物的潜力。
