- 期刊
- OpenAccess
葉酸營養狀熊以及活化巨噬細胞對肝癌胞株移勤性之影響
Effects of Folate and Macrophages Activation on Migration of Human Hepatocellular Carcinoma Cell Lines
摘要
The aim of this study was to investigate the effects of folate status on the migration of hepatocellular carcinoma (HCC) cells in the presence and absence of inflammation. Three HCC cell lines (HepG2, Hep3B, and SK-Hep-1) were used as the experiment models. Cells were preincubated with folate-deficient or folate-supplemented medium (7nM, 10µM, and 100µM) for 4 days and challenged with/without inflammation conditions using activated macrophage-conditioned medium (AMCM). Cellular migration was determined by a wound-healing assay. Folate deficiency significantly inhibited the migration of SK-Hep-1 by 25% (~P＜0.05). Compared to the folate-deficient group, folate supplementation at 7 nM, 10µM, and 100µM concentrations increased SK-Hep-1 migration by 1.09-,' 1.28-, and 1.21-fold (~P＜0.05), respectively. The migration of HepG2 cells decreased by 3% with folate deficiency, and folate supplementation restored the migration capability of HepG2 cells. In contrast, the folate status did not affect Hep3B migration. Treatment of SK-Hep-1, HepG2, and Hep3B cells with AMCM for 24 h promoted cellular migration by 1.06-, 1.1-, and 1.16-fold, respectively (p~＜0.05). Folate deficiency reduced AMCM-induced migration of SK-Hep-1 cells by 29%, and folate supplementation increased the migration level to that similar to the controls. AMCM-induced motility of HepG2 cells decreased with folate deficiency. With folate supplementation, AMCM also significantly stimulate HepG2 migration. Folate deficiency inhibited AMCM-induced migration of Hep3B cells by 12%, but there was no effect on Hep3B migration with folate supplementation. In summary, our results indicate that the folate status differently modulated HCC cell migration capabilities in the presence or absence of inflammation. Further experiments are needed to elucidate how these interactions are regulated.
並列摘要
The aim of this study was to investigate the effects of folate status on the migration of hepatocellular carcinoma (HCC) cells in the presence and absence of inflammation. Three HCC cell lines (HepG2, Hep3B, and SK-Hep-1) were used as the experiment models. Cells were preincubated with folate-deficient or folate-supplemented medium (7nM, 10µM, and 100µM) for 4 days and challenged with/without inflammation conditions using activated macrophage-conditioned medium (AMCM). Cellular migration was determined by a wound-healing assay. Folate deficiency significantly inhibited the migration of SK-Hep-1 by 25% (~P＜0.05). Compared to the folate-deficient group, folate supplementation at 7 nM, 10µM, and 100µM concentrations increased SK-Hep-1 migration by 1.09-,' 1.28-, and 1.21-fold (~P＜0.05), respectively. The migration of HepG2 cells decreased by 3% with folate deficiency, and folate supplementation restored the migration capability of HepG2 cells. In contrast, the folate status did not affect Hep3B migration. Treatment of SK-Hep-1, HepG2, and Hep3B cells with AMCM for 24 h promoted cellular migration by 1.06-, 1.1-, and 1.16-fold, respectively (p~＜0.05). Folate deficiency reduced AMCM-induced migration of SK-Hep-1 cells by 29%, and folate supplementation increased the migration level to that similar to the controls. AMCM-induced motility of HepG2 cells decreased with folate deficiency. With folate supplementation, AMCM also significantly stimulate HepG2 migration. Folate deficiency inhibited AMCM-induced migration of Hep3B cells by 12%, but there was no effect on Hep3B migration with folate supplementation. In summary, our results indicate that the folate status differently modulated HCC cell migration capabilities in the presence or absence of inflammation. Further experiments are needed to elucidate how these interactions are regulated.
延伸閱讀
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