Ginsenoside M1 Induces Apoptosis and Inhibits the Migration of Human Oral Cancer Cells

• Published in: International journal of molecular sciences Vol. 21; no. 24; p. 9704
• Main Authors: Lee, Yu-Chieh, Wong, Wei-Ting, Li, Lan-Hui, Chu, Lichieh Julie, Menon, Mridula P, Ho, Chen-Lung, Chernikov, Oleg V, Lee, Sheau-Long, Hua, Kuo-Feng
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 19.12.2020; MDPI
• Subjects: Animals; Annexin V; Apoptosis; Biotransformation; Cancer therapies; caspase; Caspase-3; Cell cycle; Cell Movement; Cell Proliferation; Chromatography; DNA damage; Fermentation; Fungi; G1 phase; ginsenoside; Ginsenosides - pharmacology; Humans; Male; Malignancy; Metabolites; Metastases; Mice; Mice, Inbred BALB C; Mice, Nude; migration; Mouth Neoplasms - drug therapy; Mouth Neoplasms - metabolism; Mouth Neoplasms - pathology; Oral administration; Oral cancer; Oral squamous cell carcinoma; p53 Protein; Physiology; Squamous cell carcinoma; Tumor Cells, Cultured; Vimentin; Xenograft Model Antitumor Assays; Xenografts; Xenotransplantation; Beijing China; United States > US; China; Taiwan; biotransformation; xenograft; ginsenoside; migration; apoptosis; oral squamous cell carcinoma; caspase
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21249704

Oral squamous cell carcinoma (OSCC) accounts for 5.8% of all malignancies in Taiwan, and the incidence of OSCC is on the rise. OSCC is also a common malignancy worldwide, and the five-year survival rate remains poor. Therefore, new and effective treatments are needed to control OSCC. In the present study, we prepared ginsenoside M1 (20-O-beta-d-glucopyranosyl-20(S)-protopanaxadiol), a major deglycosylated metabolite of ginsenoside, through the biotransformation of leaves by the fungus SP-LSL-002. We investigated the anti-OSCC activity and associated mechanisms of ginsenoside M1 in vitro and in vivo. We demonstrated that ginsenoside M1 dose-dependently inhibited the viability of human OSCC SAS and OEC-M1 cells. To gain further insight into the mode of action of ginsenoside M1, we demonstrated that ginsenoside M1 increased the expression levels of Bak, Bad, and p53 and induced apoptotic DNA breaks, G1 phase arrest, PI/Annexin V double-positive staining, and caspase-3/9 activation. In addition, we demonstrated that ginsenoside M1 dose-dependently inhibited the colony formation and migration ability of SAS and OEC-M1 cells and reduced the expression of metastasis-related protein vimentin. Furthermore, oral administration or subcutaneous injection of ginsenoside M1 significantly reduced tumor growth in SAS xenograft mice. These results indicate that ginsenoside M1 can be translated into a potential therapeutic against OSCC.