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IGF-1 induces the epithelial-mesenchymal transition via Stat5 in hepatocellular carcinoma

Chuanzong Zhao, Qian Wang, Ben Wang, Qi Sun, Zhaobin He, Jianguo Hong, Florian Kuehn, Enyu Liu _ and Zongli Zhang

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Oncotarget. 2017; 8:111922-111930. https://doi.org/10.18632/oncotarget.22952

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Chuanzong Zhao1, Qian Wang2, Ben Wang1, Qi Sun1, Zhaobin He1, Jianguo Hong1, Florian Kuehn3, Enyu Liu1 and Zongli Zhang1

1Department of General Surgery, Qilu Hospital of Shandong University, Jinan, P.R. China

2Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, P.R. China

3Department of General, Thoracic, Vascular and Transplantation Surgery, University of Rostock, Rostock, Germany

Correspondence to:

Enyu Liu, email: [email protected]

Zongli Zhang, email: [email protected]

Keywords: IGF-1; Stat5; EMT; HCC

Received: August 18, 2017     Accepted: November 17, 2017     Published: December 05, 2017


It has been reported that the epithelial-mesenchymal transition (EMT) plays an important role in hepatocellular carcinoma (HCC). However, the relationship between the insulin-like growth factor-1 (IGF-1) and EMT of HCC was not fully elucidated. In the present work, we found that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively associated with IGF-1R expression, while E-cadherin expression was negatively associated with IGF-1 expression in human HCC samples. Furthermore, we observed that IGF-1 up-regulated the expression of N-cadherin, Vimentin, Snail1, Snail2 and Twist1, and down-regulated the expression of E-cadherin. In addition, Stat5 was induced in IGF-1-treated HepG2 and Hep3B cells, and Stat5 inhibition or siRNA significantly affected IGF-1-induced EMT in HepG2 and Hep3B cells. In conclusion, IGF-1 induces EMT of HCC via Stat5 signaling pathway. Thus, IGF-1/Stat5 can be recommended as a potential and novel therapeutic strategy for HCC patients.

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