The Studies To Anti-tumor Effect And Its Mechanisms Of Trichostatin On Human Colon Cancer HCT-116 Cell Line In Vitro

Objective:To Study the Anti-Tumor Effect and its Mechanisms of trichostatin A on Human Colon Cancer HCT-116 Cell Line In Vitro.Methods: In vitro,human colon cancer cell line HCT-116 were treated with trichostatin A by means of CCK8 assay,the absorbance value was detected and growth inhibition rate was calculated.Cell cycle and apoptosis was assessed by flow cytometry,Western Blot was taken to detect DMTF1,CyclinD1,Bid and acetylated histone3 protein expression.Results:CCK8 assay indicated that the inhibitory effect of different concentrion (75ng/ml,150ng/ml,300ng/ml,600ng/ml)trichostatin A on the proliferation of HCT-116 cell was found in dose-and-time dependent manner.There was great statistical signification between varies medicated group and control group(P<0.05),and there also were great statistical signification between medicated group each other(P<0.05).Flow cytometry showed that the HCT-116 cell cycle was induced by trichostatin A at 48 hours,the ratio of G0/G1 phase was increased and the ratio of S phase was decreased significantly (P<0.05). meanwhile, The proportion of apoptosis of trichostatin A (75,150,300,600ng/ml) group in the 48h was(4.6±0.55)%,(37.06±7.89)%,(71.2±5.55)%,(75.93±3.28)%,respectively, which were all significantly higher than the blank control group(P<0.05). Western blotting indicated that trichostatin A can down- regulate the expression of CylinD1,up-regulate the expression of DMTF1,bid and acetylated histone3 in cell.Conclusion: Arichostatin A could inhibit the growth of HCT-116 cell in dose-and-time dependent maner. It could also induce HCT-116 cell apoptosis and arrest cell cycle at the phase of G0/G1.TSA on the HCT-116 colon cancer cell growth inhibition may block the cell cycle,inducing apoptosis and down-regulate the expression of CylinD1,up-regulate the expression of DMTF1,Bid and acetylated histone3 and so on.