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NOP7 interacts with β-catenin and activates β-catenin/TCF signaling in hepatocellular carcinoma cells

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 w...

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Detalles Bibliográficos
Autores principales: Wu, Nan, Zhao, Jing, Yuan, Youhua, Lu, Chuanjia, Zhu, Wenjing, Jiang, Qun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6171516/
https://www.ncbi.nlm.nih.gov/pubmed/30319277
http://dx.doi.org/10.2147/OTT.S164601
Descripción
Sumario: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.