Effect of ORP8 on proliferation, migration and invasion of colorectal cancer cells DLD-1

Acta Universitatis Medicinalis Anhui 2021 06 v.56 904-908     font:big middle small

Found programs:

Authors:Pan Qiwei; Chen Weicong; Pei Dongsheng

Keywords:ORP8;colorectal cancer;epithelial-mesenchymal transition;proliferation;migration;invasion

DOI:10.19405/j.cnki.issn1000-1492.2021.06.013

〔Abstract〕 Objective To observe and analyze the effect of ORP8 protein on the proliferation, migration and invasion ability of human colorectal cancer DLD-1 cells, and to preliminarily explore the mechanism of its influence. Methods The expression levels of ORP8 in colorectal cancer were up-regulated and down-regulated by transfection of ORP8 expression plasmid or ORP8 siRNA in colorectal cancer DLD-1 cell. The effects of interference or overexpression on the proliferation,migration and invasion of colorectal cancer cell DLD-1 were detected by CCK-8 test,transwell test and wound healing test. Western blot was used to detect the total protein and phosphorylation levels of ORP8 in the extracellular regulated protein kinases( ERK1/2) and the expression of epithelial-mesenchymal transition( EMT) related molecular markers protein E-cadherin,N-cadherin and Vimentin are studied. Results In colorectal cancer cell line DLD-1,when ORP8 was silenced,the cell proliferation,migration and invasion capacity significantly increased( P<0. 01),the expression levels of epithelial marker E-cadherin decreased,the expression levels of mesenchymal marker Vimentin and N-cadherin increased,and the expression level of p-ERK1/2 also increased. On the contrary,when ORP8 was overexpressed,the cell proliferation,migration and invasion capacity significantly decreased,the expression levels of epithelial marker E-cadherin increased( P<0. 01、P<0. 01、P<0. 05),the expression levels of mesenchymal marker N-cadherin and Vimentin protein decreased,and the expression level of p-ERK1/2 also decreased. Conclusion ORP8 protein can inhibit the proliferation,migration and invasion of colorectal cancer cell DLD-1,and its molecular mechanism may be related to blocking EMT transformation and inhibition of phosphorylation of p-ERK1/2.