CXCL12调控PI3K/AKT信号通路抑制肝癌细胞hepG2凋亡

CXCL12 regulates PI3K/AKT signaling pathway to inhibit liver cancer cell hepG2 apoptosis

目的探讨CXCL12对肝癌hepG2细胞凋亡的影响及其分子机制。方法采用流式细胞术(FCM)检测CXCL12对hepG2细胞凋亡的影响,采用Western blot及激光共聚焦(LSCM)检测CXCL12对hepG2细胞凋亡蛋白的影响及PI3K抑制剂LY294002的作用;采用Western blot检测CXCL12对PI3K/AKT信号通路的影响及PI3K抑制剂LY294002的作用。结果 100 ng/ml CXCL12可抑制hepG2细胞的凋亡,下调Bax蛋白表达,上调Bcl-2蛋白的表达;100 ng/ml CXCL12不影响p110β、p85及AKT蛋白的总表达,增加p-p85、p-AKT(ser473)蛋白的表达。PI3K抑制剂LY294002可以阻断CXCL12抑凋亡的作用,上调Bax蛋白表达,下调Bcl-2蛋白的表达;PI3K抑制剂LY294002不影响p110β、p85及AKT蛋白的总表达,减少CXCL12诱导的p-p85、p-AKT(ser473)蛋白的表达。结论 CXCL12可以上调Bcl-2/Bax比值、抑制hep G2细胞的凋亡,其作用机制可能与活化PI3K/AKT信号通路有关。

Objective To investigate the role of CXCL12 on hepG2 cells apoptosis and its molecular mechanism. Methods hepG2 cells apoptosis was detected by flow cytometry(FCM), protein expression involving hepG2 apoptosis was detected by Western blot and laser scanning confocal microscopy(LSCM), protein expression of PI3 K/AKT signaling pathway was detected by Western blot. Results 100 ng/ml CXCL12 had an ability in inhibiting hepG2 cells apoptosis, down-regulating the protein expression of Bax, up-regulating the protein expression of Bcl-2, p-p85 and p-AKT(ser473), while had no effect on the protein expression of p110β, p85 and AKT. The inhibitor of PI3 K(LY294002) blocked the anti-apoptosis effect of CXCL12, increased the protein expression of Bax, decreased the protein expression of Bcl-2, p-p85 and p-AKT(ser473), while had no effect on the protein expression of p110β, p85 and AKT. Conclusion CXCL12 can increase the ratio of Bcl-2/Bax, inhibit hepG2 cells apoptosis, and the potential mechanism may be related to the activation of PI3 K/AKT signaling pathway.