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. 2016 May 12;21(5):626. doi: 10.3390/molecules21050626

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© 2016 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic representation of the inhibitory effects of ITCs on EMT and invasion-metastatic mechanism in PCa cells in vitro. (a) During EMT epithelial cells decrease adhesion, change their morphology, polarity and position. EMT is characterized by a dowregulation (↓ bold arrow) and upregulation (↑ bold arrow) of genes that are characteristic of an epithelial and mesenchymal phenotype, respectively; The invasive (b) and migration (c) capacities are increased in the cells overexpressing CXCR4, MMP-2, MMP-9, MMP-3 (↑ bold arrow). Inhibitory effects of ITCs are represented by blue arrows (↑, enhanced expression, activity or protein levels; ↓, reduced expression, activity or protein levels). Abbreviations: BITC, benzyl isothiocyanate; BM, basement membrane; CXCR4, chemokine receptor type 4; ECM, extracellular matrix; EMT, epithelial- mesenchymal transition; MMP-2, matrix metalloproteinases (gelatinase-A); MMP-9, matrix metalloproteinases (gelatinase-B); PEITC, phenethyl isothiocyanate; SFN, sulforaphane; SFN-NAC, N-acetylcysteine conjugate of sulforaphane; TJs, tight junctions.