Proline-rich protein 11 silencing inhibits hepatocellular carcinoma growth and epithelial-mesenchymal transition through β-catenin signaling.

Proline-rich protein 11 (PRR11) has been shown to play an critical roles in the development of cancer. However, the clinical significance and the biological role of PRR11 in hepatocellular carcinoma (HCC) remains unknown. The present study aimed to investigate the expression pattern, prognostic value and the biological role of PRR11 in HCC. PRR11 expression in 80 HCC surgical specimens was examined, and its clinical significance was analyzed. The role of PRR11 in cell proliferation, colony formation, migration and invasion were also determined. The results showed that PRR11 mRNA was significantly up-regulated in 56.25% (45/80) HCC from that in matched adjacent non-tumor tissues. High PRR11 was correlated with tumor size (P = 0.01) and TNM stage (P = 0.006). Patients with higher PRR11 expression had poor overall survival time (P < 0.001). Furthermore, PRR11 silencing obviously inhibited cell proliferation, colony formation, as well as cell migration and invasion of HCC cell lines in vitro. Mechanistically, knockdown of PRR11 significantly decreased the expression of β-catenin, cyclinD1, c-myc and N-cadherin in HCC cell lines. Additionally, the inhibitory effects of PRR11 silencing on cell migration was significantly enhanced by β-catenin inhibition. PRRl1 mRNA expression was found positively correlated with β-catenin (R = 0.5472, P ˂ 0.0001), c-myc (R = 0.5527, P ˂ 0.0001) and cyclinD1 (R = 0.3948, P = 0.0003) in HCC tissues. Collectively, our data demonstrate that PRR11 plays an oncogenic role in HCC progression, through activating the Wnt/β-catenin signaling pathway, and may represent a valuable prognostic marker and therapeutic target for HCC.

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