1. 12‑Lipoxygenase promotes invasion and metastasis of human gastric cancer cells via epithelial‑mesenchymal transition
- Author
-
Jian-Ying Li, Zhixin Chen, Xiazhong Wang, Fenglin Chen, Mingkai Zhuang, Yue-Hong Huang, and Canmei Zhong
- Subjects
0301 basic medicine ,Cancer Research ,Cell ,epithelial-mesenchymal transition ,Biology ,medicine.disease_cause ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,medicine ,metastasis ,12-lipoxygenase ,Epithelial–mesenchymal transition ,gastric carcinoma ,integumentary system ,Oncogene ,Cancer ,Articles ,invasion ,medicine.disease ,Molecular medicine ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Carcinogenesis - 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
- Published
- 2018
- Full Text
- View/download PDF