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目的探讨扶正抗癌方(FZKAF)对体外培养的人肝癌细胞Hep G2迁移与侵袭能力的影响及可能的机制。方法将细胞随机分为实验组和对照组,实验组给予FZKAF处理,对照组不添加任何药物,用MTT法测定两组Hep G2细胞的活力,再分别采取细胞-基质黏附实验、划痕实验、Transwell侵袭及迁移实验测定Hep G2细胞黏附,侵袭及迁移的能力;最后通过明胶酶谱实验测定Hep G2细胞内TGF-β1的酶活性。结果 FZKAF能抑制Hep G2细胞的增殖,呈浓度依赖性,细胞-基质黏附实验、划痕实验、Transwell侵袭及迁移实验表明实验组细胞的黏附,侵袭及迁移的能力明显低于对照组(P<0.05);明胶酶谱实验显示,随着FZKAF浓度的增加可以明显抑制Hep G2细胞内TGF-β1的酶活性。结论一定剂量的FZKAF在体外可以抑制Hep G2细胞的粘附,迁移和侵袭,其机制可能是通过抑制TGF-β1的酶活性,抑制其表达,从而阻断肿瘤细胞的EMT过程有关。
Objective To investigate the effects of Fuzheng anticancer drug (FZKAF) on migration and invasion of Hep G2 cells cultured in vitro and its possible mechanism. Methods The cells were randomly divided into experimental group and control group. FZKAF was used in the experimental group, and no drug was added in the control group. The viability of Hep G2 cells in both groups was determined by MTT assay. Cell-matrix adhesion assay, scratch test, Transwell invasion and migration assays were used to determine the ability of Hep G2 cells to adhere, invade and migrate. Finally, the enzyme activity of TGF-β1 in Hep G2 cells was determined by gelatin zymography. Results FZKAF could inhibit the proliferation of Hep G2 cells in a concentration-dependent manner. The cell-matrix adhesion assay, scratch test, Transwell invasion assay and migration assay showed that the adhesion, invasion and migration ability of FZKAF was significantly lower than that of the control group (P < 0.05). Gelatin zymography showed that the FZKAF concentration significantly inhibited the activity of TGF-β1 in Hep G2 cells. Conclusion A certain dose of FZKAF can inhibit the adhesion, migration and invasion of Hep G2 cells in vitro. The mechanism may be through inhibiting the enzyme activity of TGF-β1 and inhibiting its expression, thereby blocking the EMT process of tumor cells.