Figure 6
From: Selective killing of K-ras–transformed pancreatic cancer cells by targeting NAD(P)H oxidase
![Figure 6](http://media.springernature.com/full/springer-static/image/art%3A10.1186%2Fs40880-015-0012-z/MediaObjects/40880_2015_12_Fig6_HTML.gif)
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.