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Pubmed ID :29548818
Publication Date : //

DRR1 promotes glioblastoma cell invasion and epithelial-mesenchymal transition via regulating AKT activation.


Metastatic invasion is the primary cause of treatment failure for GBM. EMT is one of the most important events in the invasion of GBM; therefore, understanding the molecular mechanisms of EMT is crucial for the treatment of GBM. In this study, high expression of DRR1 was identified to correlate with a shorter median overall and relapse-free survival. Loss-of-function assays using shDRR1 weakened the invasive potential of the GBM cell lines through regulation of EMT-markers. The expressions of p-AKT were significantly decreased after DRR-depletion in SHG44 and U373 cells. Moreover, the invasion was inhibited by the AKT inhibitor, MK-2206. The expression of Vimentin, N-cadherin, MMP-7, snail and slug was significantly inhibited by MK-2206, while the expression of E-cadherin was upregulated. Our results provide the first evidence that DRR1 is involved in GBM invasion and progression possibly through the induction of EMT activation by phosphorylation of AKT.

Authors : Ma Yu-Shui , Wu Zhi-Jun , Bai Rui-Zhen , Dong Hua , Xie Bing-Xue , Wu Xiao-Hong , Hang Xiao-Sheng , Liu Ai-Ning , Jiang Xiao-Hui , Wang Gao-Ren , Jiang Jun-Jian , Xu Wen-Huan , Chen Xiao-Ping , Tan Guang-Hong , Fu Da , Liu Ji-Bin , Liu Quan ,

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