KAP-1 is overexpressed and correlates with increased metastatic ability and tumorigenicity in pancreatic cancer.

Abstract

This study aimed to investigate the role in metastasis and prognostic value of KAP-1 in pancreatic cancer (PC). The expression of KAP-1 was analyzed by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical staining in 91 human PC tissue samples. Capan-2 cells were transfected with a lentiviral vector expressing KAP-1 (Capan-2/KAP-1) or the empty vector (Capan-2/vector); cell migration and invasion were assayed in vitro using Transwell migration and wound-healing assays, and in vivo using a xenograft model in nude mice. KAP-1 was found to be overexpressed in human PC, and the expression of KAP-1 correlated with clinical stage. Overexpression of KAP-1 increased the invasion and migration of Capan-2 cells in vitro. Furthermore, overexpression of KAP-1 promoted the growth and metastatic ability of PC cells in a xenograft model in nude mice. Moreover, overexpression of KAP-1 induced the epithelial-mesenchymal transition (EMT) in PC cells both in vitro and in vivo, as indicated by increased expression of mesenchymal markers such as vimentin and decreased expression of E-cadherin. This study indicates that KAP-1 may promote metastasis in PC by regulating the EMT and suggests that KAP-1 may have potential as a predictor of metastasis in patients with pancreatic cancer.