中国医科大学学报2018，Vol.47Issue(2)：151-156,6.DOI:10.12007/j.issn.02584646.2018.02.013
Hedgehog/Gli和PI3K/AKT信号通路的串话促进胃癌AZ521细胞上皮—间质转化
Crosstalk of Hedgehog/Gli and PI3k/Akt Pathway Promotes Epithelial-mesenchymal Transition in Gastric Adenocarcinoma
摘要
Abstract
Objective To investigate the tumor molecular mechanism of Hedgehog/Gli in promoting the epithelial-mesenchymal transition (EMT) in gastric cancer AZ521 cells. Methods After 24 h of treatment with GANT61,the mRNA expression of Gli1,Gli2, N-cadherin,and E-cadherin in the AZ521 cell line were detected by real-time fluorescence quantitative PCR. A Western blotting assay was conducted to determine the expression of the above cytokines,p-AKT and AKT. The effect of GANT61 on invasion was observed by transwell assay. N-Shh stimulation of the Hedgehog pathway was conducted to confirm the changes in these cytokines. Results GANT61 significantly downregulated the mRNA expression of Gli1,Gli2,and N-cadherin,but upregulated E-cadherin mRNA expression. The Western blotting assay revealed that GANT61 downregulated the protein expression of Gli1,Gli2,p-AKT,and N-cadherin,but upregulated E-cadherin expression. Furthermore,GANT61 inhibited the invasion. N-Shh proteins up-regulated Gli1,Gli2,and N-cadherin mRNA,protein expression and p-AKT protein expression,but downregulated E-cadherin mRNA and protein expressions. N-Shh promoted the invasion of tumor cells. Conclusion Downregulation of Gli1 and Gli2 can inhibit the invasion and metastasis in gastric cancer cells,which may be related to the promotion of EMT by Gli through the PI3K/AKT pathway.关键词
胃癌/Hedgehog/Gli/PI3K/AKT/GANT61/上皮-间质转化Key words
gastric adenocarcinoma/Hedgehog/ Gli/PI3K/AKT/GANT61/epithelial-mesenchymal transition分类
医药卫生引用本文复制引用
王雷,杜媛鲲,米源,廖海江,陈阁,张耀中,刘庆熠..Hedgehog/Gli和PI3K/AKT信号通路的串话促进胃癌AZ521细胞上皮—间质转化[J].中国医科大学学报,2018,47(2):151-156,6.基金项目
河北省科技厅科技攻关计划(132077127D) （132077127D）
河北省卫计委医学重点科研基金(20160177) （20160177）
