G‑protein‑coupled receptor 120 regulates the development and progression of human esophageal cancer.

The aim of the present study was to investigate the role of G‑protein coupled receptor 120 (GPR120) in esophageal cancer and explore the related mechanisms. The expression of GPR120 in esophageal cancer tissues was examined by immunohistochemistry. Correlation analysis was performed to investigate the association between the level of GPR120 and clinical parameters. The expression of GPR120 was evaluated in esophageal cancer cell lines and the effects of GPR120 on cell proliferation, clone formation, migration and invasion were evaluated in an in vitro cell model and an in vivo ectopic tumor nude mice model. In addition, the effect of GPR120 on epithelial‑mesenchymal transition (EMT), PI3K and I‑κB pathway, as well as angiogenesis and inflammation‑related cytokines was explored in order to elucidate the underlying mechanisms. Significantly increased expression of GPR120 was observed in esophageal cancer tissues compared to normal tissues. The expression of GPR120 was significantly related with histological grade, TNM stage and lymph node metastasis. GPR120 knockdown significantly decreased cell proliferation, clone formation, migration and invasion in vitro and decreased tumor growth in vivo. Furthermore significantly increased levels of E‑cadherin and decreased levels of N‑cadherin and vimentin, decreased level of Akt phosphorylation and I‑κB phosphorylation, as well as decreased levels of vascular endothelial growth factor (VEGF), interleukin‑8 (IL‑8) and cyclooxygenase‑2 (Cox‑2) and its corresponding protein PGE2 were observed as the underlying mechanisms. In conclusion, we observed an increased level of GPR120 in esophageal cancer tissues, which served as a positive regulator of the development and progression of esophageal cancer. Multiple mechanisms including EMT, PI3K and I‑κB pathway, as well as angiogenesis and inflammation‑related cytokines were involved.