scholarly journals 979 Zoledronic acid sensitizes renal cell carcinoma cells to radiation by downregulating STAT1

2013 ◽  
Vol 12 (1) ◽  
pp. e979-e980
Author(s):  
T. Kijima ◽  
F. Koga ◽  
Y. Fujii ◽  
S. Yoshida ◽  
M. Tatokoro ◽  
...  
2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Toshiki Kijima ◽  
Fumitaka Koga ◽  
Yasuhisa Fujii ◽  
Soichiro Yoshida ◽  
Manabu Tatokoro ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64615 ◽  
Author(s):  
Toshiki Kijima ◽  
Fumitaka Koga ◽  
Yasuhisa Fujii ◽  
Soichiro Yoshida ◽  
Manabu Tatokoro ◽  
...  

2012 ◽  
Vol 10 (8) ◽  
pp. 1109-1119 ◽  
Author(s):  
Ming-Yi Ho ◽  
Shye-Jye Tang ◽  
Mei-Jen Chuang ◽  
Tai-Lung Cha ◽  
Jing-Yao Li ◽  
...  

2011 ◽  
Vol 22 (8) ◽  
pp. 749-762 ◽  
Author(s):  
Nicoletta Gagliano ◽  
Letizia Pettinari ◽  
Massimo Aureli ◽  
Carla Martinelli ◽  
Elena Colombo ◽  
...  

Author(s):  
Haitao Song ◽  
Yanwei Rao ◽  
Gang Zhang ◽  
Xiangbo Kong

MicroRNAs (miRNAs) are emerging as pivotal regulators in the development and progression of various cancers, including renal cell carcinoma (RCC). MicroRNA-384 (miR-384) has been found to be an important cancer-related miRNA in several types of cancers. However, the role of miR-384 in RCC remains unclear. In this study, we aimed to investigate the potential function of miR-384 in regulating tumorigenesis in RCC. Here we found that miR-384 was significantly downregulated in RCC tissues and cell lines. Overexpression of miR-384 significantly inhibited the growth and invasion of RCC cells, whereas inhibition of miR-384 had the opposite effects. Bioinformatic analysis and luciferase reporter assay showed that miR-384 directly targeted the 3′-untranslated region of astrocyte elevated gene 1 (AEG-1). Further data showed that miR-384 could negatively regulate the expression of AEG-1 in RCC cells. Importantly, miR-384 expression was inversely correlated with AEG-1 expression in clinical RCC specimens. Moreover, miR-384 regulates the activation of Wnt signaling. Overexpression of AEG-1 significantly reversed the antitumor effects of miR-384. Overall, these findings suggest that miR-384 suppresses the growth and invasion of RCC cells via downregulation of AEG-1, providing a potential therapeutic target for the treatment of RCC.


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