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NOP7 interacts with β-catenin and activates β-catenin/TCF signaling in hepatocellular carcinoma cells
Authors Wu N, Zhao J, Yuan Y, Lu C, Zhu W, Jiang Q
Received 4 February 2018
Accepted for publication 23 June 2018
Published 1 October 2018 Volume 2018:11 Pages 6369—6376
DOI https://doi.org/10.2147/OTT.S164601
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 4
Editor who approved publication: Dr Samir Farghaly
Nan Wu,1 Jing Zhao,2,3 Youhua Yuan,4 Chuanjia Lu,1 Wenjing Zhu,1 Qun Jiang1
1Department of Clinical Laboratory, Shanghai Stomatological Hospital, Fudan University, Shanghai, People’s Republic of China; 2Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China; 3Cancer Metastasis Institute, Fudan University, Shanghai, People’s Republic of China; 4Department of Clinical Laboratory, Henan Provincial People’s Hospital, Zhengzhou, People’s Republic of China
Background: The hyperactivation of β-catenin signaling is frequently observed in clinical hepatocellular carcinoma (HCC) samples. Further understanding the mechanisms involved in activating β-catenin/TCF signaling would benefit the treatment of HCC.
Method and results: Here, it was found that NOP7 was a binding partner of β-catenin. NOP7 strengthened the interaction between β-catenin and TCF4, which led to the activation of β-catenin/TCF signaling. The upregulation of NOP7 in HCC promoted the growth (in both liquid culture and soft agar) and migration of HCC cancer cells.
Conclusion: Taken together, we have demonstrated the oncogenic functions of NOP7 in HCC, suggesting that targeting NOP7 would benefit the treatment of HCC.
Keywords: hepatocellular carcinoma, NOP7, β-catenin/TCF pathway, cell growth, cell migration
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