Nrdp1-mediated degradation of BRUCE decreases cell viability and induces apoptosis in human 786-O renal cell carcinoma cells

被引:4
|
作者
Chen, Shao-Jun [1 ]
Lin, Jian-Hai [1 ]
Yao, Xu-Dong [1 ]
Peng, Bo [1 ]
Xu, Yun-Fei [1 ]
Liu, Min [1 ]
Zheng, Jun-Hua [1 ]
机构
[1] Tongji Univ, Shanghai Peoples Hosp 10, Dept Urol, 301 Yanchang Rd, Shanghai 200072, Peoples R China
基金
中国国家自然科学基金;
关键词
Nrdp1; BRUCE; renal cell carcinoma; viability; apoptosis; CANCER CELLS; NRDP1; IAP; PROLIFERATION; EXPRESSION; PATHWAY; PROTEIN; GROWTH; GENE;
D O I
10.3892/etm.2016.3356
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Neuregulin receptor degradation protein-1 (Nrdp1) is involved in a plethora of cellular processes and plays an essential role in the development and progression of human cancers. However, its role in renal cell carcinoma (RCC) remains unclear. Therefore, the present study aimed to explore the biological significance of Nrdp1 in RCC. Western blot analyses of tissue samples from 24 patients with primary RCC revealed lower Nrdp1 and higher baculovirus inhibitor of apoptosis repeat-containing ubiquitin-conjugating enzyme (BRUCE) protein levels in RCC tissues compared with adjacent normal tissues. In addition, MTT and apoptosis assays demonstrated that Nrdp1 overexpression resulted in decreased cell viability and enhanced apoptosis in RCC 786-O cells; conversely, Nrdp1 knockdown increased 786-O cell viability and inhibited apoptosis. Further analysis showed that BRUCE downregulation partially attenuated the effects of Nrdp1 knockdown on RCC cell viability and apoptosis. Moreover, an inverse association was obtained between BRUCE and Nrdp1 protein levels. These findings suggest that Nrdp1-mediated degradation of BRUCE decreases cell viability and induces apoptosis in RCC cells, highlighting Nrdp1 as a potential target for RCC treatment.
引用
收藏
页码:597 / 602
页数:6
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