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. 2015 Sep 27;6(34):35522–35541. doi: 10.18632/oncotarget.5849

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Copyright: © 2015 Liu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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A. NDRG1 inhibits Src activity and its downstream signaling pathway. B. Line drawings of the structures of potential anti-metastatic agents under development. A. NDRG1 expression inhibits c-Src phosphorylation at its activating site (Tyr416). This occurs through NDRG1-induced reduction in EGFR expression, abrogation of EGF-mediated EGFR activation, and thus preventing the EGFR-c-Src interaction. Moreover, NDRG1 was shown to suppress Rac1 activity by modulating the phosphorylation of a c-Src down-stream effector, namely p130Cas and its association with CrkII, which acts as a molecular switch to activate Rac1. B. Line drawings of: Genistein, KISS1-derived peptide, etoposide, atrasentan, di-2-pyridylketone 4,4,-dimethyl-3-thiosemicarbazone (Dp44mT) and di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone (DpC).