中文摘要：

目的：探讨细胞外热休克蛋白70（HSP70）/HSP70肽复合物（HSP70-PCs）对肝癌细胞上皮-间充质转化（EMT）的影响和可能机制。方法：将HepG2细胞分为3组：正常对照组、HSP70/HSP70-PCs组（终浓度2 mg/L）和LY294002＋HSP70/HSP70-PCs组。应用real-time RT-PCR与Western blotting法检测上皮细胞表面标志E-cadherin和间质细胞表面标志α-平滑肌肌动蛋白（α-SMA）的表达变化，以及磷脂酰肌醇3-激酶（PI3K）和缺氧诱导因子1α（HIF1-α）的表达变化。结果：细胞外HSP70/HSP70-PCs可以促进HepG2细胞EMT的发生。HepG2细胞的EMT过程伴随HIF-1α和PI3K表达增加。应用LY294002阻断PI3K后，HepG2细胞没有发生EMT，同时细胞外HSP70/HSP70-PCs上调HIF-1α表达的作用消失。结论：细胞外HSP70/HSP70-PCs可以通过PI3K/HIF-1α促进肝癌细胞发生EMT。

英文摘要：

AIM：To investigate the effect of extracellular heat-shock protein 70 （HSP70）/HSP70-peptide complexes （HSP70-PCs） on epithelial-mesenchymal transition （EMT） of human hepatocellular carcinoma HepG2 cells and its probable mechanism. METHODS：HepG2 cells were divided into 3 groups： control group, HSP70/HSP70-PCs （2 mg/L） group and LY294002＋HSP70/HSP70-PCs group. The mRNA and protein expression of epithelial cell surface marker E-cadherin, mesenchymal cell surface marker α-smooth muscle actin （α-SMA）, phosphatidylinositol 3-kinase （PI3K） and hypoxia-inducible factor 1α （HIF-1α） was examined by real-time RT-PCR and Western blotting. RESULTS：Extracellular HSP70/HSP70-PCs promoted the initiation of EMT of HepG2 cells. The expression of HIF-1α and PI3K significantly increased in the process of EMT of HepG2 cells. After PI3K was blocked by LY294002, EMT did not occur and HIF-1α was not up-regulated in HepG2 cells. CONCLUSION：Extracellular HSP70/HSP70-PCs may promote EMT of hepatocellular carcinoma cells via PI3K/HIF-1α signaling pathway.