Galectin-1 induces invasion and the epithelial-mesenchymal transition in human gastric cancer cells via non-canonical activation of the hedgehog signaling pathway
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Yang Chong1, Dong Tang1, Jun Gao1, Xuetong Jiang1, Chuanqi Xu1, Qingquan Xiong1, Yuqin Huang1, Jie Wang1, Huaicheng Zhou1, Youquan Shi1, Daorong Wang1
1Department of Gastrointestinal Surgery, Clinical Medical College of Yangzhou University, Subei People’s Hospital of Jiangsu Province, Yangzhou 225001, China
Daorong Wang, email: firstname.lastname@example.org
Keywords: galectin-1, epithelial-mesenchymal transition, hedgehog signaling, Gli-1, gastric cancer
Received: May 20, 2016 Accepted: October 21, 2016 Published: November 08, 2016
Galectin-1 (Gal-1) has been reported to be an independent prognostic indicator of poor survival in gastric cancer and overexpression of Gal-1 enhances the invasiveness of gastric cancer cells. However, the downstream mechanisms by which Gal-1 promotes invasion remains unclear. Moreover, the function of Gal-1 in the epithelial-mesenchymal transition (EMT) in gastric cancer has not yet been elucidated. In this study, we observed Gal-1 expression was upregulated and positively associated with metastasis and EMT markers in 162 human gastric cancer tissue specimens. In vitro studies showed Gal-1 induced invasion, the EMT phenotype and activated the non-canonical hedgehog (Hh) pathway in gastric cancer cell lines. Furthermore, our data revealed that Gal-1 modulated the non-canonical Hh pathway by increasing the transcription of glioma-associated oncogene-1 (Gli-1) via a Smoothened (SMO)-independent manner, and that upregulation of Gal-1 was strongly associated with gastric cancer metastasis. We conclude that Gal-1 promotes invasion and the EMT in gastric cancer cells via activation of the non-canonical Hh pathway, suggesting Gal-1 could represent a promising therapeutic target for the prevention and treatment of gastric cancer metastasis.
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