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. 2018 May 6;10(5):137. doi: 10.3390/cancers10050137

Figure 5.

Figure 5

Schematic representation of the pharmacological compounds (black boxes) that inhibit YAP and TAZ oncogenic function through targeting YAP and TAZ or the main proteins and pathways that influence YAP and TAZ in lung cancer. Honokiol reactivates LKB1 and inhibits the YAP/TAZ/β-catenin oncogenic pathway. Statins and norcantharidin (NCTD) inhibit the mevalonate pathway and the production of monounsaturated fatty acids—two biosynthetic pathways of lipids that are increased in tumorigenesis. Through the inhibition of these two pathways, statins and norcantharidin inhibit oncogenic YAP, TAZ, and β-catenin signaling. Statins also inhibit EGFR autophosphorylation and β-catenin activation and nuclear translocation. Rottlerin is a natural polyphenolic compound which inhibits oncogenic TAZ in lung. EGFR inhibitors are too many to be listed here, but they inhibit the EGFR receptors and their downstream effectors and their inhibition has a synergistic effect when combined with YAP inhibition mediated by Verteporfin. This latter impairs the binding of YAP with the oncogenic transcription factors TEADs. Black arrows indicate pharmacological activation of the targeted proteins or pathways. Black blunt lines indicate pharmacological inhibition of the targeted proteins or pathways. As in previous figures, lines or arrows in red indicate signals which eventually activate nuclear YAP/TAZ, while lines or arrows in blue indicate signals or proteins which eventually inhibit nuclear YAP/TAZ, through mechanisms either dependent on or independent of Hippo pathway core kinases. Dashed arrows indicate reciprocal crosstalk between receptors and their downstream transduction.