PI3K/Akt信号通路对肝癌细胞系HepG2中SP细胞的影响

[目的]探讨PI3K/Akt信号通路对肝癌细胞系HepG2中肿瘤干细胞比例及干细胞特性的影响.[方法]使用PI3K/Akt通路抑制剂处理HepG2细胞后,使用流式技术分析HepG2细胞系中的侧群（SP）细胞的变化.软琼脂克隆形成实验检测PI3K/Akt抑制剂对HepG2细胞中SP细胞和非SP细胞成克隆能力的影响.[结果]HepG2细胞中存在SP细胞,经过LY294002处理后,SP细胞比例下降.LY294002可以显著降低SP细胞的软琼脂成克隆能力,对非SP细胞的软琼脂成克隆能力影响不明显.[结论]HepG2细胞中的SP细胞具有干细胞特性,PI3K/Akt信号通路对HepG2细胞中SP细胞的维持起重要作用,抑制PI3K/Akt信号通路后HepG2细胞中的SP细胞比例明显减低,并能显著抑制SP细胞的增殖速度、软琼脂成克隆能力,增加SP细胞对化疗药物的敏感性,为更加深入地了解肝癌干细胞的特性以及探索针对肿瘤干细胞的治疗提供理论依据.

Effects of PI3K/Akt signaling pathway on SP cells in hepatocellular carcinoma cell line HepG2

[Objective]To investigate the effect of PI3K/Akt pathway on the ratio and character of canc- er stem cells in hepatocellular carcinoma（HCC）cell line HepG2 cells. [Methods]Changes of SP cells in HepG2 cells was analyzed by fluorescence activated cell sorter after HepG2 cells were administrated by in- hibitor of PI3K/Akt pathway. Soft agarose assay was used to detect the effect of PI3K/Akt pathway inhib- itor on the colone ability of sp cells and non SP cells in HepG2 cells. [Results]SP cells existed in HepG2 cell line,and the ratio of SP cells was decreased after treated by PI3K/Akt inhibitor. LY294002 inhibited the cell proliferation and the colony forming ability of SP cells significantly but had no effect on that of non-SP cells. [Conclusion]SP cells in HepG2 showed property of stem cell,and PlaK/Akt pathway was im- portant to the maintenance of SP cell in HepG2 cells. Inhibition of PI3K/Akt pathway reduced SP ratio in HepG2 cells and inhibited the proliferation and colony forming ability of SP cells, and also increased the sensibility of SP cells responding to chemotherapeutics. These results may provide proof for further under- standing of the property of hepatoma stem cells and exploration of treatment targeting cancer stem cells.