J Cancer 2018; 9(15):2650-2658. doi:10.7150/jca.25188
Pentraxin 3 overexpression accelerated tumor metastasis and indicated poor prognosis in hepatocellular carcinoma via driving epithelial-mesenchymal transition
Department of Hepatobiliary Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China
As a pattern recognition receptor, pentraxin 3 (PTX3) has been found to exert the pleiotropic roles on a variety of cancers. However, the accurate clinical significance of PTX3 in hepatocellular carcinoma (HCC) has not been well defined. The aim of the present investigation was to determine the expression characteristics, prognostic significance, and the relevant biological effect of PTX3 in HCC. The expression of PTX3 was evaluated in tumor and adjacent liver tissues from 210 HCC patients using immunohistochemistry staining. And it was found that a marked up-regulation in the expression of PTX3 in the HCC specimens, which was remarkably correlated with high serum AFP level (P = 0.006), larger tumor size (P <0.001), liver cirrhosis (P = 0.004), advanced TNM stage (P = 0.022), PVTT (P = 0.010), intra-hepatic metastases (P = 0.019), and MVI (P <0.001). PTX3 was identified as an independent predictive factor of poor prognosis by multivariate analysis. Ectopic expression of PTX3 enhanced proliferation, migration, invasion capacities of Huh7 cells and induced EMT phenotype. Silencing PTX3 obtained the opposite results. Moreover, the in vivo experiments confirmed PTX3 induced EMT and promoted proliferation and growth of HCC cells. Collectivelly, these data indicated that PTX3 could accelerate HCC progression through activating EMT and served as a potential predictive factor and therapeutic target for HCC.
Keywords: PTX3, HCC, EMT, prognosis, predictive factor
Song T, Wang C, Guo C, Liu Q, Zheng X. Pentraxin 3 overexpression accelerated tumor metastasis and indicated poor prognosis in hepatocellular carcinoma via driving epithelial-mesenchymal transition. J Cancer 2018; 9(15):2650-2658. doi:10.7150/jca.25188. Available from http://www.jcancer.org/v09p2650.htm