@Article{096504016X14774889687280,
AUTHOR = {Zhenhua Zhao, Hui Liu, Junqing Hou, Tieqiang Li, Xinyi Du, Xiaolei Zhao, Wenchao Xu, Weibo Xu, Junkai Chang},
TITLE = {Tumor Protein D52 (TPD52) Inhibits Growth and Metastasis in Renal Cell  Carcinoma Cells Through the PI3K/Akt Signaling Pathway},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {5},
PAGES = {773--779},
URL = {http://www.techscience.com/or/v25n5/56859},
ISSN = {1555-3906},
ABSTRACT = {Tumor protein D52 (TPD52) is a member of the TPD52-like protein family and plays different roles in various types of malignancies. However, its role in renal cell carcinoma (RCC) is still unclear. In this study, we 
investigated the role of TPD52 in RCC. The mechanism of TPD52 in RCC was also investigated. Our data 
demonstrated that the expression levels of TPD52 in both mRNA and protein were significantly decreased 
in RCC cells. Overexpression of TPD52 inhibited proliferation, migration, and invasion with decreased 
epithelial–mesenchymal transition (EMT) phenotype in RCC cells, as well as attenuated tumor growth in 
renal cancer xenografts. Mechanistically, overexpression of TPD52 significantly inhibited downregulated 
phosphorylation levels of PI3K and Akt in RCC cells. In conclusion, the present study demonstrated that 
TPD52 inhibited growth and metastasis of RCC, at least in part, by suppressing the PI3K/Akt signaling 
pathway. Therefore, these findings suggest that TPD52 may be a promising therapeutic target for the treatment of human RCC.},
DOI = {10.3727/096504016X14774889687280}
}