FOXM1 facilitates gastric cancer cell migration and invasion by inducing Cathepsin D
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Li Yang1,*, Ming Cui2,*, Liang Zhang3 and Lei Song3
1Department of Intensive Care Unit, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
2Department of Emergency, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
3Department of Interventional Therapy, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
*Li Yang and Ming Cui contributed equally to this work as the co-first author.
Liang Zhang, email: firstname.lastname@example.org
Lei Song, email: email@example.com
Keywords: FOXM1, Cath-D, gastric cancer
Received: March 14, 2017 Accepted: June 09, 2017 Published: July 15, 2017
Forkhead box M1 (FOXM1) has been reported as a vital transcription factor in different human malignancies. To date, the mechanisms of FOXM1 in modulating the invasion and metastasis of gastric cancer cells have not been elucidated. In the present study, we found that overexpression of FOXM1 prompted cell migration and invasion of gastric cancer, and increased the expression of Cathepsin D (Cath-D). However, FOXM1 siRNA repressed cell migration and invasion, and also decreased the expression of Cath-D in gastric cancer cells. Blocking of Cath-D repressed FOXM1 overexpression-mediated cell migration and invasion. Mechanically, FOXM1 facilitated the activation of Cath-D promoter. Furthermore, overexpression of Cath-D affected the expression of E-cadherin, leading to epithelial-mesenchymal transition (EMT) of gastric cancer cells. In conclusion, this study demonstrated that FOXM1 promotes gastric cancer cell migration and invasion through inducing expression of Cath-D in gastric cancer. Thus, FOXM1 may be recommended as a potential therapeutic target for gastric cancer patients.
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