ABSTRACT
Purpose To investigate the expression of LI-cadherin in advanced gastric cancer and its effect and mecha-nism on human gastric cancer cell line MKN28. Methods Im-munohistochemical staining was performed on advanced gastric cancer to examine the LI-cadherin protein expression. CCK8, colony formation assay, transwell assay, flow cytometry were used to detect the changes in the biological behavior of MKN28 cells after LI-cadherin gene interference. Dual-luciferase report-er assay and Western blot were used to detect the activity of the NF-κB after the interference of LI-cadherin gene. Results LI-cadherin in chronic gastritis was negative, in well- and moder-ately-differentiated advanced gastric cancer was significantly in-creased, in poorly-differentiated was decreased. Cell prolifera-tion, colony formation, and invation ability were inhibited in the group of knockdown expression of LI-cadherin ( P ＜ 0. 05 ). Flow cytometry results showed that knockdown expression of LI-cadherin resulted in a significant increase in the proportion of cells in G1 phase, while the proportion of cells in S phase was significantly lower ( P ＜0. 05 ). Knockdown expression of LI-cadherin resulted in the decreased activation of NF-κB and re-stricted its translation. Conclusion LI-cadherin in well- and moderately-differentiated advanced gastric cancer is significantly increased. Knockdown of LI-cadherin can strongly decrease the malignant biological characteristics of human gastric cancer cell line MKN28. Its mechanism may be associated with the NF-κB pathway.