@Article{096504016X14719078133203,
AUTHOR = {Xiangfei He, Fuguang Sun, Fengfu Guo, Kai Wang, Yisheng Gao, Yanfei Feng, Bin Song, Wenzhi Li, Yang Li},
TITLE = {Knockdown of Long Noncoding RNA FTX Inhibits Proliferation, Migration, and Invasion in Renal Cell Carcinoma Cells},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {2},
PAGES = {157--166},
URL = {http://www.techscience.com/or/v25n2/56794},
ISSN = {1555-3906},
ABSTRACT = {Renal cell carcinoma (RCC) is one of the most common kidney cancers worldwide. Although great progressions have been made in the past decades, its morbidity and lethality remain increasing. Long noncoding RNAs 
(lncRNAs) are demonstrated to play significant roles in the tumorigenesis. This study aimed to investigate the 
detailed roles of lncRNA FTX in RCC cell proliferation and metastasis. Our results showed that the transcript 
levels of FTX in both clinical RCC tissues and the cultured RCC cells were significantly upregulated and 
associated with multiple clinical parameters of RCC patients, including familial status, tumor sizes, lymphatic 
metastasis, and TNM stages. With cell proliferation assays, colony formation assays, and cell cycle assays, 
we testified that knockdown of FTX in A498 and ACHIN cells with specific shRNAs inhibited cell proliferation rate, colony formation ability, and arrested cell cycle in the G<sub>0</sub>
/G<sub>1</sub>
 phase. FTX depletion also suppressed 
cell migration and invasion with Transwell assays and wound-healing assays. These data indicated the prooncogenic potential of FTX in RCC, which makes it a latent therapeutic target of RCC diagnosis and treatment 
in the clinic.},
DOI = {10.3727/096504016X14719078133203}
}