白藜芦醇对缺氧诱导胃癌细胞的上皮间质转化的抑制作用及其可能机制

Inhibitive effect and its possible mechanism of resveratrol on epithelial-mesenchymal transition of gastric carcinoma cells induced by hypoxia

目的本研究探讨白藜芦醇对缺氧诱导胃癌细胞的上皮间质转化(epithelial-mesenchymal transition,EMT)的抑制作用及其可能机制。方法在缺氧和正常情况下培养胃癌细胞SGC-7901,设立对照组、白藜芦醇组、缺氧组、白藜芦醇+缺氧组,通过四甲基偶氮唑盐比色(MTT)法检测白藜芦醇对胃癌细胞的增生抑制作用,细胞划痕试验检测白藜芦醇对胃癌细胞侵袭转移的抑制作用,荧光定量PCR(RT-qPCR)、蛋白免疫印迹法(Western Blot)检测胃癌细胞中上皮间质转化相关因子Snail、E-cadherin及vimentin的表达情况。结果与对照组相比,缺氧状态下胃癌细胞SGC-7901的侵袭和转移能力显著增强,缺氧状态下,E-cadherin的表达降低,而Snail和vimentin的表达升高,白藜芦醇则可以抑制缺氧的影响,且白藜芦醇的抑制作用主要表现为对HIF-1α蛋白表达的影响,而对HIF-1α mRNA无影响。结论白藜芦醇可能通过影响HIF-1α蛋白的表达,抑制胃癌细胞的增生、侵袭及上皮间质转化过程。

Objective To explore the inhibitive effect and its possible mechanism of resveratrol on epithelial-mesenchymal transition（EMT） of gastric carcinoma cells induced by hypoxia.Me thods Gastric carcinoma SGC-7901 cells were cultured under hypoxic condition and normal conditions.The control group,the resveratrol group,the hypoxia group and resveratrol＋ hypoxia group were established.The methabenzthiazuron（MTT） assay was used to evaluate the inhibitive effect on proliferation of SGC-7901 cells.The wound scratch assay was adopted to determine the inhibitive effect of resveratrol on the migration ability of gastric carcinoma cells.PCR（RT-qPCR） and Western Blot analysis were used to detect the expression of epithelial-mesenchymal transition related factors in gastric cancer cellssnail,such as E-cadherin and vimentin protein levels.Re s ults Compared with the control group,hypoxia significantly increased the proliferation rate and invasive ability of SGC-7901 cells.Moreover,hypoxia markedly decreased the E-cadherin level and increased Snail and vimentin expression.However,resveratrol reversed all the above effects of hypoxia in SGC-7901 cells.Moreover,resveratrol inhibited HIF-1α protein accumulation without affecting the HIF-1α mRNA level.Conclus ion Resveratrol could inhibit the proliferation,invasion and epithelial-mesenchymal transition process in gastric carcinoma cells via affecting the accumulation of the HIF-1α protein.