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. 2015 Apr 8;34:8. doi: 10.1186/s40880-015-0012-z

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© Wang et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Proposed model of the selective killing of K-ras –transformed cells by NOX inhibition. K-ras transformation causes the activation of the downstream effector, phosphatidylinositol 3′-kinase (PI3K). Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), the lipid product of a PI3K-catalyzed reaction, enhances the guanine-nucleotide exchange factor (GEF) activity that mediates the exchange of Rac-GDP for Rac-GTP, and provides the lipid necessary for NOX subunit (p40phox) binding upon the translocation to the membrane, therefore causing the activation of NOX. NOX-induced ROS production stimulates cell proliferation and contributes to tumor progression. NOX inhibitor targets the activated NOX and causes excessive ROS generation, leading to cancer cell death. +, activation by the upstream effectors.