Abstract: Background and purpose: Previous studies have confirmed that the expression of leucine-rich repeat-containing 3B (CLRRC3B) was significantly decreased in different human cancers, which was also associated with the migration and invasion of cancer cells. The aim of this study was to explore the potential mechanism of LRRC3B in the development of esophageal cancer. Methods: The LRRC3B expression was detected in 60 cancer tissues and 60 adjacent non-neoplastic tissues by immunohistochemistry. The mRNA and protein expression of LRRC3B in Eca109 and HEECs were detected using real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot, respectively. Eca109 cells with different treatments were divided into three groups: normal group, negative control group (transfected with pCMV6 plasmid), overexpression LRRC3B group (transfected with pCMV6-LRRC3B plasmid). Transwell assay was used to measure the migration and invasion of Eca109 cells in different groups. The protein levels of E-cadherin, N-cadherin, Vimentin and p-Akt were determined by Western blot. Results: The expression of LRRC3B in esophageal cancer tissues was lower than that of non-cancerous tissues, as well as the expression of LRRC3B in Eca109 was decreased compared with that of normal esophageal epithelial cell line HEEC. Overexpression of LRRC3B significantly inhibited Eca109 cells migration and invasion, upregulated the expression of E-cadherin and decreased the expression of N-cadherin and Vimentin. Moreover, overexpression of LRRC3B significantly inhibited the phosphorylation of Akt in Eca109 cells. Conclusion: The expression of LRRC3B was decreased in esophageal cancer. Overexpression of LRRC3B can efficiently inhibit the EMT progression in esophageal cancer cells by suppressing PI3K/Akt signaling pathway.

Key words: Leucine-rich repeat-containing 3B, Esophageal cancer, Epithelial-mesenchymal transition, PI3K/Akt