2018OncoTargets and TherapyOpen access

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

Nan Wu, Jing Zhao, Youhua Yuan, Chuanjia Lu, Wenjing Zhu, Qun Jiang

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Abstract

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.

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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.

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Available abstract

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.

Key concepts: Hepatocellular carcinoma, Beta-catenin, BETA (programming language), Cancer research, Catenin, Signal transduction, Medicine, Chemistry

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