Jun Yang1, Junquan Liu2, Xiaoting Lyu2, Sujuan Fei1. 1. Department of Gastroenterology, Affiliated Hospital, Xuzhou Medical College, Xuzhou 221004, China. 2. Central Laboratory, Chinese PLA 97 Hospital, Xuzhou 221004, China.
Abstract
OBJECTIVE: To investigate the effect of resveratrol (Res) on the proliferation, apoptosis and immunogenicity of colorectal cancer stem cells (CCSCs). METHODS: The CCSCs were induced from colon cancer cell line HCT116 in serum-free medium (SFM). The expressions of CD133 and CD44 were detected by flow cytometry to identify CCSCs. After treatment with Res at (12.5-200.0) μmol/L, the effect of Res on CCSC proliferation was detected by MTT assay ; cell apoptosis was examined by flow cytometry combined with annexin V-FITC/PI staining; cell cycle and the expression of major histocompatibility complex class I-related chain A and B (MICA/B) were assessed by flow cytometry. RESULTS: HCT116 cells formed cancer stem cell spheres in SFM. The proportion of CD133⁺ cells in cell spheres was (91.07 ± 1.79)%, and CD44⁺ cells was (90.33 ± 1.78)%. Compared with control groups, Res significantly inhibited CCSC proliferation in a time- and dose-depended manner. After treatment with Res for 48 hours, the proportion of cells increased in the G0/G1 phase and decreased in the S phase, both in a dose-depended manner. Apoptosis rate of CCSCs and the expression of MICA/B were raised with the increasing concentration of Res. CONCLUSION: CCSCs were successfully induced from HCT116 colon cancer cell line. Res could depress CCSC proliferation in a time-and dose-depended manner, arrest cell cycle in the G0/G1 phase and promote cell apoptosis. Res could up-regulate the expression of MICA/B in CCSCs and enhance cell immunogenicity.
OBJECTIVE: To investigate the effect of resveratrol (Res) on the proliferation, apoptosis and immunogenicity of colorectal cancer stem cells (CCSCs). METHODS: The CCSCs were induced from colon cancer cell line HCT116 in serum-free medium (SFM). The expressions of CD133 and CD44 were detected by flow cytometry to identify CCSCs. After treatment with Res at (12.5-200.0) μmol/L, the effect of Res on CCSC proliferation was detected by MTT assay ; cell apoptosis was examined by flow cytometry combined with annexin V-FITC/PI staining; cell cycle and the expression of major histocompatibility complex class I-related chain A and B (MICA/B) were assessed by flow cytometry. RESULTS: HCT116 cells formed cancer stem cell spheres in SFM. The proportion of CD133⁺ cells in cell spheres was (91.07 ± 1.79)%, and CD44⁺ cells was (90.33 ± 1.78)%. Compared with control groups, Res significantly inhibited CCSC proliferation in a time- and dose-depended manner. After treatment with Res for 48 hours, the proportion of cells increased in the G0/G1 phase and decreased in the S phase, both in a dose-depended manner. Apoptosis rate of CCSCs and the expression of MICA/B were raised with the increasing concentration of Res. CONCLUSION: CCSCs were successfully induced from HCT116 colon cancer cell line. Res could depress CCSC proliferation in a time-and dose-depended manner, arrest cell cycle in the G0/G1 phase and promote cell apoptosis. Res could up-regulate the expression of MICA/B in CCSCs and enhance cell immunogenicity.