FBXL20 promotes cell proliferation and metastasis through activating Wnt/β-catenin signaling pathway in esophageal cancer

Previous studies have demonstrated that FBXL20 can promote tumor progression in human colorectal adenocarcinoma. Additionally, FBXL20, acts as a checkpoint of p53, controls autophagy and receptor degradation. These studies suggest that FBXL20 is involved in several cancer progression. However, the role of FBXL20 in esophageal cancer remains unknown. The present study demonstrated that the expression of FBXL20 in esophageal cancer tissue was significantly higher than its expression in adjacent tissues. In vitro studies, silencing FBXL20 expression by lentiviral vector shRNA induced G0/G1 cell cycle arrest, and inhibited the proliferation, migration and invasion ability of esophageal cancer cells through Wnt/beta-catenin signaling pathway. In addition, FBXL20 silencing could increase the apoptosis of esophageal cancer cells. In summary, this study demonstrated that FBXL20 was an oncogenic gene, which could promote proliferation, migration, invasion, and G0/G1 cell cycle arrest via activating Wnt/beta-catenin signaling pathway and induce apoptosis in esophageal cancer. Therefore, FBXL20 might serve as a potential tumor marker and therapeutic target for esophageal cancer.