Sesamin induces cell cycle arrest and upregulation of NKG2D ligands in MG‑63 cells and increases susceptibility to NK cell cytotoxicity.
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Osteosarcoma is a common solid malignancy in children and adolescents. Despite a success of standard therapeutic approaches, an effective therapeutic strategy is in a great need for improved outcomes. The aim of the present study was to investigate the anticancer effect of sesamin and its influence on NKG2D ligand expression in human osteosarcoma MG-63 cells and to compare the differences in NK cell elimination efficiency before and after treatment. Cell viability of MG-63 cells treated with serial concentrations of sesamin (0-100 µM) was measured using MTT. Induction of cell cycle arrest was determined with flow cytometry. Flow cytometry and reverse transcription-quantitative PCR were employed to detect the changes of protein and mRNA level of NKG2D ligands before and after treatment with sesamin. NK cell elimination assay was performed to determine the changes in NK cell-mediated cytotoxicity against MG-63 cells treated with sesamin. Sesamin induced G2/M cell cycle arrest in MG-63 cells with increased p21 expression. Expression of MICA, MICB and ULBP1 at the protein and mRNA level were significantly increased (P<0.05). MG-63 cells treated with sesamin were more susceptible to NK cell-mediated elimination (P<0.05). Enhanced NK cell-mediated cytotoxicity was correlated with expression of NKG2D ligands (P<0.05). In conclusion, sesamin can induce cell cycle arrest and upregulate the expression of NKG2D ligands in MG-63 cells, thereby enhancing NK cell-mediated cytotoxicity against osteosarcoma cells.