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- W2789286023 abstract "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." @default.
- W2789286023 created "2018-03-29" @default.
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- W2789286023 date "2018-06-01" @default.
- W2789286023 modified "2023-10-15" @default.
- W2789286023 title "DRR1 promotes glioblastoma cell invasion and epithelial-mesenchymal transition via regulating AKT activation" @default.
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- W2789286023 doi "https://doi.org/10.1016/j.canlet.2018.03.015" @default.
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