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

被引:7
|
作者
Wu, Nan [1 ]
Zhao, Jing [2 ,3 ]
Yuan, Youhua [4 ]
Lu, Chuanjia [1 ]
Zhu, Wenjing [1 ]
Jiang, Qun [1 ]
机构
[1] Fudan Univ, Shanghai Stomatol Hosp, Dept Clin Lab, Shanghai, Peoples R China
[2] Fudan Univ, Huashan Hosp, Dept Gen Surg, Shanghai, Peoples R China
[3] Fudan Univ, Canc Metastasis Inst, Shanghai, Peoples R China
[4] Henan Prov Peoples Hosp, Dept Clin Lab, Zhengzhou, Henan, Peoples R China
来源
ONCOTARGETS AND THERAPY | 2018年 / 11卷
关键词
hepatocellular carcinoma; NOP7; beta-catenin/TCF pathway; cell growth; cell migration; BIOGENESIS; YTM1; COMPLEX; GROWTH; AXIN1; ERB1;
D O I
10.2147/OTT.S164601
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: The hyperactivation of beta-catenin signaling is frequently observed in clinical hepatocellular carcinoma (HCC) samples. Further understanding the mechanisms involved in activating beta-catenin/TCF signaling would benefit the treatment of HCC. Method and results: Here, it was found that NOP7 was a binding partner of beta-catenin. NOP7 strengthened the interaction between beta-catenin and TCF4, which led to the activation of beta-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.
引用
收藏
页码:6369 / 6376
页数:8
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