[Expression of PLOD2 in esophageal squamous cell carcinoma and its correlation with invasion and metastasis].

Objective: To investigate PLOD2 expression in esophageal squamous cell carcinoma, and to explore the potential mechanism by which PLOD2 promotes tumor metastasis. Methods: The expression of PLOD2 in 60 cases of esophageal squamous cell carcinoma (the patients were collected at the first Affiliated Hospital of Xinxiang Medical University, from January 2016 to December 2017) was investigated by immunohistochemistry. Fibrillar collagen formation and collagen deposition were detected by picrosirius red staining. Correlation of PLOD2 expression with clinical pathologic features of the patients was performed using χ(2) test and Kaplan-Meier analysis. After EC-109 cells were transfected with LV-vector and LV-over/PLOD2, the expression of PLOD2 was detected by real time PCR and the impact of POLD2 on invasion in EC-109 cells was determined by transwell migration and invasion assays. The expression of PLOD2/AKT epithelial-to-mesenchymal transition signal pathway related proteins was detected by Western blot. Results: The expression level of PLOD2 in esophageal squamous cell carcinoma was 81.7% (49/60 cases),higher than their paired noncancerous tissues(8.3%, 5/60; P<0.01), and correlated significantly with tumor depth of invasion and nodal metastasis (P<0.01). Picrosirius red staining showed that collagen deposition was increased and the degree of fibrillar organization was enhanced in carcinoma tissues that had higher PLOD2 expression. Transwell migration and invasion assays showed that PLOD2 significantly promoted the migration and invasion ability of EC-109 cells. Western blot showed that PLOD2 significantly increased the expression levels of p-FAK, p-AKT and vimentin in EC-109 cells. Conclusions: Esophageal squamous cell carcinoma has a high expression of PLOD2 that correlates with tumor invasion and lymph node metastasis. PLOD2 promotes invasion and metastasis of esophageal squamous cell carcinoma through epithelial-to-mesenchymal transition via FAK/AKT signal pathway.