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In the present study, we aimed to investigate the involvement of Snail inNF-κB-mediated changes of E-cadherin in gastric cancer. A total of 189 human gastriccancer tissues, and 32 normal gastric mucosal tissues were used to determine theexpression levels of NF-κB, E-cadherin and Snail by immunohistochemistry. Thecorrelation between the expression levels and patient clinicopathological datawas analyzed. Human gastric cancer cell line SGC7901 was treated with the NF-κBinhibitor PDTC, and the expression levels of E-cadherin and Snail were investigatedby qPCR and western blot. NF-κB, E-cadherin and Snail were all detected in normalgastric mucosa and cancer tissues of various differentiation statuses. However,the expression patterns of each protein were different. Strong expression of E-cadherinwas detected in normal gastric mucosa, whereas its expression gradually declinedin gastric cancer tissues, with weak expression observed in poorly differentiatedgastric cancer tissues. In contrast, weak NF-κB and Snail expressions were presentin normal gastric mucosa, while their expression levels gradually increased ingastric cancer tissues, with the strongest expression detected in poorly differentiatedgastric cancers. The expression of E-cadherin was inversely correlated with thatof Snail and NF-κB in the tissues tested. Blockade of NF-κB using its inhibitorPDTC led to a time-dependent reduction in Snail but a time-dependent increasein E-cadherin in SGC7901 cells. These results suggest that in human gastric cancer,loss of E-cadherin may be mediated through NF-κB-induced Snail upregulation. Furtherstudies may reveal whether targeting the NF-κB-Snail-E-cadherin axis could bea useful approach for combating gastric cancer.

Possible regulatory role of Snail in NF-κB-mediated changes in E-cadherin in gastric cancer