GPI-PLD 通过下调PI3K-Akt 信号通路活性抑制肝癌细胞的生长

目的：明确糖基化磷脂酰肌醇特异性磷酯酶D (glycosylphosphatidylinositol-specific phospholipase D，GPIPLD)对肝癌细胞HepG2 的影响以及可能的调控分子机制。方法：通过转染构建高表达GPI-PLD 模型，利用MTT、荧光染色以及Western 印迹检测高表达GPI-PLD 对肝癌细胞的影响，同时接种于裸鼠模型中，进一步明确GPI-PLD在体内对肝癌细胞的影响。结果：与空白组和对照组相比，GPI-PLD 组PI3K-Akt 信号通路活性明显受到抑制，肝癌细胞增殖活性明显受到抑制并呈现典型的凋亡形态。肝癌裸鼠模型结果显示GPI-PLD 组肿瘤的生长速度、肿瘤质量[(1.87±0.09) g] 小于空白组[(2.20±0.17) g] 和对照组[(2.15±0.09) g]，GPI-PLD 组AST，ALT，AFP 血清浓度显著低于空白组和对照组(P<0.05)。结论：GPI-PLD 可通过下调PI3K-Akt 信号通路活性，抑制肝癌细胞的增殖及体内生长，促进肝癌细胞的凋亡。

GPI-PLD inhibits the growth of hepatoma cells by down-regulation of PI3K-Akt signaling pathway

Objective: To clarify the effect of glycosylphosphatidylinositol-specific phospholipase D (GPIPLD)on hepatoma cells HepG2 and the possible molecular mechanism.Methods: MTT, fluorescent staining and Western blot were applied to analyze the effect andmolecular mechanism of GPI-PLD on hepatoma cells by transfected high expression GPI-PLDmodel. We inoculated HepG2 in nude mice models to further clarify the effect of GPI-PLD onhepatoma cells in vivo.Results: Compared with the control groups, PI3K-Akt signaling pathway activity and proliferationof hepatoma cells were significantly inhibited in the GPI-PLD group. Nude mice models showedthat the tumor growth and tumor weight [(1.87±0.09) g] of the GPI-PLD group were significantlyless than those of the blank control group [(2.20 ± 0.17) g] and the negative control group [(2.15±0.09) g]. AST, ALT and AFP serum concentration in the GPI-PLD group were significantly lowerthan those of the control groups (P<0.05).Conclusion: GPI-PLD can inhibit the proliferation of hepatoma cells and growth in vivo, andpromote the apoptosis of hepatoma cells by reducing the activity of PI3K-Akt signaling pathway.