Abstract
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.
Highlights
Gastric cancer is the fifth most common malignant tumor type and third-leading cause of cancer-related deaths worldwide [1]
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
Upregulation of Gal-1 is clinically associated with the epithelialmesenchymal transition (EMT) and metastasis in human gastric cancer
Summary
Gastric cancer is the fifth most common malignant tumor type and third-leading cause of cancer-related deaths worldwide [1]. More than 90 percent of cancer-related deaths among patients with solid tumors are not the result of the primary tumor, but due to the metastasis and invasion of secondary tumors in different organs [2]. Metastatic progression, the spread of primary tumors to distant organs, is a complex, multistep physiological process. A large number of studies have shown the epithelialmesenchymal transition (EMT) plays a critical important role in tumor cell invasion and metastasis, and leads to upregulation of mesenchymal genes such as Vimentin and downregulation of epithelial-associated markers such as E-cadherin [3]. As a result of the EMT, tumor cells acquire metastatic and invasive properties, exhibit characteristics that resemble embryonic mesenchymal cells, and have enhanced ability to penetrate the surrounding stroma to initiate the formation of new neoplastic foci [4, 5]
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