PT - JOURNAL ARTICLE AU - HAIBO ZHANG AU - JUNKOO YI AU - EUNGYUNG KIM AU - YEONSIK CHOO AU - HUANG HAI AU - KIRIM KIM AU - EUN-KYONG KIM AU - ZAEYOUNG RYOO AU - MYOUNGOK KIM TI - 20(S)-Ginsenoside Rh2 Suppresses Oral Cancer Cell Growth by Inhibiting the Src-Raf-ERK Signaling Pathway AID - 10.21873/anticanres.14769 DP - 2021 Jan 01 TA - Anticancer Research PG - 227--235 VI - 41 IP - 1 4099 - http://ar.iiarjournals.org/content/41/1/227.short 4100 - http://ar.iiarjournals.org/content/41/1/227.full SO - Anticancer Res2021 Jan 01; 41 AB - Background: 20(S)-Ginsenoside Rh2 (G-Rh2) has demonstrated therapeutic effects in many types of cancers. We aimed to investigate the potential anticancer activity and underlying mechanisms of G-Rh2 in oral cancer cells. Materials and Methods: The antigrowth effect of G-Rh2 in oral cancer cells was stimulated by cell proliferation, soft agar colony formation, and migration and invasion assay. The cell cycle and apoptosis were detected by flow cytometry. The underlying mechanism of G-Rh2 in oral cancer cells was explored by immunoblotting. Results: G-Rh2 significantly inhibited oral cancer cell growth by inducing apoptosis and cell cycle G0/G1-phase arrest. G-Rh2 inhibited oral cancer cell migration and invasion through regulation of epithelial–mesenchymal transition (EMT)-related proteins. G-Rh2 inhibited the Src/Raf/ERK signaling pathway in YD10B and Ca9-22 cells. Conclusion: G-Rh2 exerted anticancer activity in vitro by inhibiting the Src/Raf/ERK signaling pathway in oral cancer. G-Rh2 is a potential therapeutic drug for oral cancer treatment.