Research Papers:

The long noncoding RNA HOTAIR activates the Hippo pathway by directly binding to SAV1 in renal cell carcinoma

Guanghui Hu, Binbin Dong, Jingwei Zhang, Wei Zhai, Tiancheng Xie, Bisheng Huang, Chi Huang, Xudong Yao, Junhua Zheng, Jianping Che and Yun-Fei Xu _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:58654-58667. https://doi.org/10.18632/oncotarget.17414

Metrics: PDF 2158 views  |   HTML 2707 views  |   ?  


Guanghui Hu1*, Binbin Dong2,*, Jingwei Zhang1,*, Wei Zhai1,3, Tiancheng Xie1, Bisheng Huang1, Chi Huang4, Xudong Yao1, Junhua Zheng1, Jianping Che1,4 and Yun-Fei Xu1

1Department of Urology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China

2Department of Urology, Yancheng Third People’s Hospital, Yancheng, Jiangsu, China

3Department of Urology, Renji Hospital, Shanghai Jiaotong University, Shanghai, China

4Department of Urology, Shanghai Tenth People’s Hospital, Nanjing Medical University, Nanjing, Jiangsu, China

*These authors have contributed equally to this work

Correspondence to:

Yun-Fei Xu, email: [email protected]

Jianping Che, email: [email protected]

Wei Zhai, email: [email protected]

Keywords: renal cell carcinoma, HOTAIR, hippo pathway, SAV1

Received: December 31, 2016    Accepted: March 14, 2017    Published: April 25, 2017


The long noncoding RNA HOTAIR promotes the development and progression of several tumors. Here, the clinical significance and role of HOTAIR in renal cell carcinoma (RCC) tumorigenesis were explored. The results showed that increased expression of HOTAIR predicted a poor prognosis of RCC after surgery. HOTAIR promoted RCC cell proliferation and growth in vitro and in vivo. The expressions of HOTAIR and Salvador homolog 1 (SAV1) were inversely correlated in clinical RCC samples. HOTAIR downregulated SAV1 by directly binding to the SAV1 protein and enhanced histone H3K27 methylation. Loss of function of SAV1 activated the Hippo pathway. HOTAIR could be a potential therapeutic target in RCC.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 17414