Silencing Neuropilin 1 gene reverses TGF-β1-induced epithelial mesenchymal transition in HGC-27 gastric cancer cell line  被引量:1

在线阅读下载全文

作  者:Weiguo Xu Xin Yang Qiqi Zhan Guanyi Ding Shang Guo Bing Zhu Hong Xu Xiangmei Liu 

机构地区:[1]Department of Surgical Oncology,North China University Of Science and Technology Affiliated Hospital,Tangshan 063000,China [2]North China University of Science and Technology,Tang Shan 063000,China [3]Department of Gynaecology and Obstetrics,Liuyang Maternal and Child Health Care Hospital,Liu Yang 410300,China

出  处:《Oncology and Translational Medicine》2020年第6期258-265,共8页肿瘤学与转化医学(英文版)

基  金:Supported by grants from Returning Overseas Students(No.CY201721).

摘  要:Objective The aim of this study was to determine Neuropilin 1(NRP1)contribution to transforming growth factorβ1(TGF-β1)-induced epithelial mesenchymal transition(EMT)of HGC-27 gastric cancer cells and study its mechanism.Methods In this study,TGF-β1 was used to induce EMT in HGC-27 cells.Further,these cells were stably transfected with siRNA targeting NRP1.Wound healing and transwell assays were used to measure cell migration and invasion,respectively.NRP1 and EMT markers were measured using quantitative real time reverse transcription polymerase chain reaction and western blotting.Results Exposure of TGF-β1 conferred a fibroblastic-like shape to cancer cells and significantly increased the expression of NRP1 in HGC-27 cells.TGF-β1 subsequently promoted migration and invasion of HGC-27 cells.Furthermore,silencing NRP1 inhibited the invasion and migration of TGF-β1-induced cells undergoing EMT.Conclusion Silencing NRP1 can inhibit cell migration,invasion,and metastasis and reverse the TGF-β1-induced EMT process of gastric cancer.

关 键 词:Neuropilin1(NRP1) epithelial-mesenchymal transition(EMT) gastric cancer transforming growth fqactor-β1 

分 类 号:R735.2[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象