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Downregulation of LKB1 suppresses Stat3 activity to promote the proliferation of esophageal carcinoma cells.

The tumor suppressor liver kinase B1 (LKB1) encodes a serine/threonine kinase. The defect in LKB1 is the primary cause of Peutz-Jeghers syndrome (PJS). Inactivation of LKB1 by mutations or loss of LKB1 expression is associated with ovarian, lung and pancreatic cancer; however, the correlation between LKB1 and esophageal carcinoma remains unknown. Thus, quantitative PCR was performed to determine the clinical significance of LKB1 expression in 60 cases of esophageal cancer and its adjacent normal epithelium. LKB1 expression was observed to significantly downregulate the accompanying cancer progression, which was verified at the protein level by western blot analysis. Furthermore, the phosphorylated signal transducer and activator of transcription 3 (Stat3) level is reversibly associated with LKB1 expression. To determine the function of LKB1 in esophageal cancer, LKB1 expression is induced in TE1 esophageal cancer cells. The results show that LKB1 overexpression suppresses the proliferation of TE1 cells, downregulates the expression of cyclin D1 and Myc and represses Stat3 phosphorylation. Suppression of cell proliferation and cyclin D1 expression by LKB1 is fully inhibited by constitutively active Stat3C coexpression, suggesting that LKB1 inhibits esophageal cancer cell proliferation through suppression of Stat3 transaction. In conclusion, downregulation of LKB1 expression suppresses Stat3 activity that may promote tumor growth during esophageal cancer progression.