12-Lipoxygenase promotes invasion and metastasis of human gastric cancer cells via epithelial-mesenchymal transition.

Abstract

The role of 12-lipoxygenase (12-LOX) in tumorigenesis has been well established in several types of human cancer, including gastric cancer. It was reported that epithelial-mesenchymal transition (EMT) contributes to tumor invasion and metastasis. However, whether 12-LOX promotes the invasion and metastasis of human gastric cancer cells via EMT remains to be elucidated. In the present study, the expression of 12-LOX and EMT markers, N-cadherin and E-cadherin, was evaluated in gastric cancer and adjacent normal mucosa samples by immunohistochemical analysis. 12-LOX-overexpressing gastric cancer cells were established via lentiviral transfection of SCG-7901 cells. Wound-healing and Transwell assays were performed to examine the regulation of cell metastasis and invasion by 12-LOX. Furthermore, the regulation of N-cadherin expression by 12-LOX was evaluated using reverse transcription-quantitative polymerase chain reaction and western blotting. The results revealed that the expression of 12-LOX and N-cadherin was significantly higher in gastric cancer compared with that in adjacent normal mucosa tissues (P<0.05). By contrast, the expression of E-cadherin was significantly decreased in gastric cancer compared with that in adjacent normal mucosa tissues (P<0.05). Furthermore, the expression of 12-LOX was positively associated with N-cadherin expression in gastric cancer tissues. 12-LOX-overexpressing gastric cancer cells exhibited significantly increased invasion and migration abilities compared with the empty vector and control groups. The expression of N-cadherin in 12-LOX-overexpressing gastric cancer cells was increased compared with that in the empty vector and control groups. The present study suggests that EMT may be involved in the promotion of the invasion and metastasis of human gastric cancer cells by 12-LOX.