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10-8M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)5 M。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。
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： normal control group, ghrelin group and Akt blocker group; ghrelin group was treated with 10-SM ghrelin and Akt blocker group with 10.8 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 ofp-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-AM/ 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.
作者
李欢庆
樊晓明
Li Huanqing;Fan Xiaoming(Department of Gastroenterology, Jinshan Hospital Affiiated to Fudan University, Shanghai, 201508, P. R, China)
出处
《老年医学与保健》
CAS
2018年第2期161-163,共3页
Geriatrics & Health Care
基金
金山区科学技术委员会(2017-3-05)
