Role of galectin-1 in urinary bladder urothelial carcinoma cell invasion through c-Jun N-terminal protein kinase pathway

Abstract

Human galectin-1 is a member of galectin family, proteins with conserved carbohydrate-recognition domains that bind galactoside. Galectin-1 is highly expressed in various tumors and participates in various oncogenic processes. However, detailed description of the function of galectin-1 in urinary bladder urothelial carcinoma has not been provided nowadays. Our previous cohort investigation demonstrated that galectin-1 is associated with tumor invasiveness and a possible independent prognostic marker of urinary bladder urothelial carcinoma. The present study was to clarify the relevance of galectin-1 expression level to tumor progression and invasion. In order to decipher a mechanism for the contribution of galectin-1 to the malignant behaviour of urinary bladder urothelial carcinoma, two bladder cancer cell lines (T24 and J82) was established with knockdown galectin-1 expression by short-hairpin siRNA. Bladder cancer cells with gelectin-1 gene silencing exhibited reduced cell proliferation, lower invasive capability and lower clonogenicity. Extensive signalling pathway studies indicated that galectin-1 participated in bladder cancer cell invasion through mediating the activity of matrix metalloproteinase 9 via Ras─Rac1─MAP/ERK kinase kinase 4─c-Jun N-terminal protein kinase─AP1 signaling pathway. Our functional analyses of gelectin-1 in urinary bladder urothelial carcinoma provided novel insight into the critical role of gelectin-1 in tumour progression and invasion. These results revealed that silencing galectin-1-mediated MAP kinase signaling pathway presented a novel strategy for bladder cancer therapy.

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