@Article{096504018X15420748671075,
AUTHOR = {Zhongyi Mu, Dan Dong, Ning Wei, Mingli Sun, Wei Wang, Yue Shao, Jian Gao, Ping Yin, Chenghai Zhao},
TITLE = {Silencing of lncRNA AFAP1-AS1 Inhibits Cell Growth and Metastasis  in Clear Cell Renal Cell Carcinoma},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {6},
PAGES = {653--661},
URL = {http://www.techscience.com/or/v27n6/48582},
ISSN = {1555-3906},
ABSTRACT = {The lncRNA AFAP1-AS1, oriented from an antisense direction to the protein-coding gene AFAP1 in the opposite strand, was upregulated in a variety of tumors and associated with poor prognosis, including lung cancer, 
breast cancer, ovarian cancer, and so on. However, the biological role of AFAP1-AS1 in clear cell renal cell 
carcinoma (ccRCC) is still unknown. We observed that AFAP1-AS1 expression was significantly upregulated 
in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. 
Knockdown of AFAP1-AS1 markedly suppressed the progression of proliferation, invasion, migration, and 
EMT in ccRCC cells. Downregulation of AFAP1-AS1 resulted in an increase in E-cadherin and a decrease in 
vimentin. Noticeably, we found that PTEN has a negative correlation with the lncRNA AFAP1-AS1 expression. Further studies verified that PTEN deficiency effectively attenuated the ability of AFAP1-AS1 in promoting ccRCC cell proliferation, invasion, migration, and EMT. Moreover, the similar biological response of 
silencing AFAP1-AS1 was observed in our ccRCC mice model. Knockdown of AFAP1-AS1 evidently suppressed tumor growth. Taken together, our results provide the evidences that silencing of AFAP1-AS1 inhibits 
cell proliferation, EMT, and metastasis through PTEN-dependent signaling, and our findings elucidate a novel 
potential therapeutic target or biomarker for the treatment of ccRCC.},
DOI = {10.3727/096504018X15420748671075}
}