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

Medical oncology (Northwood, London, England) (2014-05-28)
Chao Yu, Lei Zhan, Jianxin Jiang, Yaozhen Pan, Hong Zhang, Xu Li, Feng Pen, Min Wang, Renyi Qin, Chenyi Sun
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.

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