饥饿激素对胃癌细胞转移的机制研究

Mechanism of Ghrelin in the Metastasis of Gastric Cancer

中文关键词: 胃肿瘤  饥饿激素  磷脂酰肌醇三激酶

英文关键词: stomach neoplasms  ghrelin  PI3K

中文摘要:

      目的 探讨饥饿激素在胃癌细胞转移中的作用及其机制.方法 将胃癌MKN-28细胞分为空白对照(normal control,NC)组、ghrelin组及Akt阻断剂组3组.Ghrelin组采用10-8 M饥饿激素处理MKN-28细胞;Akt阻断剂组在ghrelin组基础上添加Akt阻断剂哌立福新(perifosine)5μM.采用划痕法与Transwell小室检测细胞的迁移和侵袭能力;Western blot法检测人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(phosphatase and tensin homolog deleted on chromosome ten,PTEN)、磷脂酰肌醇三激酶(phosphatidylinositol 3-kinase,PI3K)、磷酸化蛋白激酶B(phosphorylated protein kinase B,p-Akt)及肌动蛋白的表达变化.结果 Ghrelin组细胞迁移和侵袭能力均高于NC组(P＜0.05),Western blot结果显示ghrelin组p-Akt与PI3K表达升高,PTEN表达下调,这种作用被哌立福新部分阻断.结论 饥饿激素可以促进胃癌细胞迁移和侵袭,p-Akt/PI3K表达上调和PTEN下调可能是饥饿激素作用的分子机制.

英文摘要:

      Objective To investigate the role of Ghrelin in the process of migration in gastric carcinoma cell.Methods Gastric MKN-28 cells were divided into 3 groups:normalcontrolgroup,ghrelin group and Akt blocker group;ghrelingroup was treated with 108M ghrelin and Akt blocker group with 10~ M ghrelin plus 5 μM perifosine;scratch test and transwell chamber were applied in measuring the ability in invasiveness and migration while western blotting was applied in detecting the expressions of p-Akt,PI3K,PTEN and Actin protein.Results The ability in invasiveness and migration in ghrelin group were higher than those in normal control group (P ＜ 0.05);western blotting showed an increase in the protein expression of p-Akt/PI3K and a decrease in the protein expression of PTEN in MKN-28 cells;in cells disposed by perifosine,these changes were reversed.Conclusion Ghrelin can promote the migration and invasiveness of gastric cancer cells,the up-regulation of p-Akt/PI3K and down-regulation of PTEN might be the molecular mechanisms of the role of ghrelin.