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机构地区:[1]延边大学医学院药理学教研室,吉林延吉133002
出 处:《延边大学医学学报》2016年第1期23-27,共5页Journal of Medical Science Yanbian University
基 金:吉林省自然科学基金(20125236)
摘 要:[目的]探讨白藜芦醇对CXCL12诱导的胃癌SGC-7901细胞迁移及侵袭的影响.[方法]利用CXCL12刺激人胃癌细胞株SGC-7901后,采用划痕法检测细胞迁移能力,进行Transwell小室体外侵袭实验检测肿瘤细胞的侵袭能力,采用RT-PCR技术检测CXCL12受体CXCR4,CXCR7mRNA及血管内皮生长因子(VEGF)mRNA表达水平,应用Western印迹技术检测细胞中p-ERK蛋白的表达.观察白藜芦醇对CXCL12诱导的SGC-7901细胞迁移及侵袭能力及CXCR4,CXCR7,VEGF mRNA,p-ERK蛋白表达的影响.[结果]CXCL12可显著促进细胞迁移及侵袭,上调CXCR4,CXCR7,VEGF mRNA及p-ERK蛋白的表达水平.白藜芦醇可明显抑制CXCL12诱导的SGC-7901细胞的迁移及侵袭,下调CXCR4,CXCR7,VEGF mRNA及p-ERK蛋白的表达水平.[结论]白藜芦醇可有效抑制CXCL12诱导的胃癌细胞的迁移及侵袭,其机制可能与下调受体CXCR4和CXCR7的表达、抑制p-ERK蛋白及VEGF mRNA的表达有关.OBJECTIVE To study the effect of resveratrol on migration and invasion of the SGC-7901 cells induced by CXCL12. METHODS SGC-7901 cells were treated with CXCL12 and resveratrol, wound healing assay and Transwell assay were performed to evaluate cells migration and invasion. The levels of CXCR4, CXCR7 and VEGF mRNA were measured by reverse transcription-polymerase chain reaction (RT-PCR), the level of p-ERK protein was measured by Western blot. RESULTS CXCL12 significantly increased migration and invasion of SGC-7901 cells, and upregulated the mRNA expression of CXCR4, CXCR7 and VEGF. Western blot assay showed that the p-ERK protein level wasalso increased by CXCL12. Resveratrol significantly inhibited migration and invasion of SGC-7901 cells induced by CXCL12, and down-regulated the expression of CXCR4, CXCR7, VEGF mRNA and p-ERK protein. CONCLUSION Resveratrol could inhibit migration and invasion of SGC-7901 cells induced by CXCL12. The mechanism may be related with the down-regulation of CXCR4, CXCR7 mRNA and VEGF mRNA expression, and inhibition of the expression of p-ERK.
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