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The crucial role of SRPK1 in IGF-1-induced EMT of human gastric cancer

Hong Wang, Chunlei Wang, Wenling Tian and Yanfen Yao _

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Oncotarget. 2017; 8:72157-72166. https://doi.org/10.18632/oncotarget.20048

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Hong Wang1, Chunlei Wang2, Wenling Tian1 and Yanfen Yao3

1Department of General Surgery, Shandong Provincial Third Hospital, Jinan, Shandong, China

2Thyroid Disease Prevention and Control Center, Shandong Provincial Institute of Endemic Disease Control, Jinan, Shandong, China

3Department of Intensive Care Unit, Shandong Provincial Third Hospital, Jinan, Shandong, China

Correspondence to:

Yanfen Yao, email: [email protected]

Keywords: SRPK1, IGF-1, EMT, GC

Received: June 28, 2017     Accepted: July 26, 2017     Published: August 07, 2017


In recent years, the insulin-like growth factor (IGF-1) and serine-arginine protein kinase 1 (SRPK1) have been reported to be implicated in the pithelial-mesenchymal transition (EMT) in many kinds of malignancies. However, the potential roles of IGF-1-SRPK1 signaling in the EMT of gastric cancer (GC) have not been investigated. In the present study, the in-vitro assays were used to investigate the molecular role of SRPK1 in cell cycle, motility and invasiveness. We demonstrated that the expressions of SRPK1 or insulin-like growth factor receptor 1 (IGF1R) were significantly increased in GC tissues and cells than those in normal tissues and GES-1 cells, and closely associated with metastasis, stage and prognosis. Western blot analysis showed that IGF-1 treatment can induce the expression of p-AKT and EMT biomarkers (N-cadherin, MMP2 and Slug) in a dose-dependent fashion in MGC803 and BGC823 cells. On the other hand, the knockdown of SRPK1 attenuated IGF-1-induced increase of EMT biomarkers and p-AKT. Besides, in-vitro analysis showed that knockdown of SRPK1 induced cell cycle arrest in G0/G1 phase, and affected cell migration and invasion. In conclusion, IGF-1-IGF1R pathway induced the expression of SRPK1 to control the progression of EMT via AKT pathway in the development of GC. Our findings lay a promising foundation for the IGF-1-IGF1R axis-targeting therapy in GC patients.

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