cIAP2 promotes gallbladder cancer invasion and lymphangiogenesis by activating the NF‐κB pathway Article Swipe
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· 2017
· Open Access
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· DOI: https://doi.org/10.1111/cas.13236
· OA: W2608859689
Several studies have produced contradictory findings about the prognostic implications for inhibitor of apoptosis proteins ( IAP ) in different types of cancer. Cellular inhibitor of apoptosis 2 ( cIAP 2/ BIRC ) is one of the most extensively characterized human IAP . To date, no studies have focused on the expression level of cIAP 2 in human gallbladder cancer ( GBC ), and the mechanism of cIAP 2 in GBC invasion and lymphangiogenesis remains unclear. Therefore, in the present study, cIAP 2 expression in GBC was detected using quantitative real‐time polymerase chain reaction and immunohistochemistry, and the relationship between cIAP 2 levels in cancer tissues and the clinicopathological characteristics of patients was analyzed. The biological effect of cIAP 2 in GBC cells was tested using the Cell Counting Kit‐8 Assay, Transwell assays and the ability of human dermal lymphatic endothelial cells ( HDLEC ) to undergo tube formation. The role of cIAP 2 in activating the NF ‐κB pathway was determined using a dual‐luciferase reporter assay, immunofluorescence staining, western blotting and ELISA . Finally, an animal model was used to further confirm the role of cIAP 2 in lymphangiogenesis. We showed that cIAP 2 expression was elevated in human GBC tissues and correlated with a negative prognosis for patients. Moreover, cIAP 2 was identified as a lymphangiogenic factor of GBC cells and, thus, promoted lymph node metastasis in GBC cells. Our study is the first to suggest that cIAP 2 can promote GBC invasion and lymphangiogenesis by activating the NF‐κB pathway.
