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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Indirubin derivatives inhibit Stat3 signaling and induce apoptosis in human cancer cells.

Stat3 protein has an important role in oncogenesis and is a promising anticancer target. Indirubin, the active component of a traditional Chinese herbal medicine, has been shown previously to inhibit cyclin-dependent kinases, resulting in cell cycle arrest. Here, we show that the indirubin derivatives E564, E728, and E804 potently block constitutive Stat3 signaling in human breast and prostate cancer cells. In addition, E804 directly inhibits Src kinase activity (IC(50) = 0.43 microM) in an in vitro kinase assay. Levels of tyrosyl phosphorylation of c-Src are also reduced in cultured cells 30 min after E804 treatment. Tyrosyl phosphorylation of Stat3, which is known to be phosphorylated by c-Src, was decreased, and constitutive Stat3 DNA binding-activity was suppressed in cells 30 min after E804 treatment. The antiapoptotic proteins Mcl-1 and Survivin, which are encoded in target genes of Stat3, were down-regulated by indirubin derivatives, followed by induction of apoptosis. These results demonstrate that E804 directly blocks the Src-Stat3 signaling pathway, suggesting that the antitumor activity of indirubin compounds is at least partially due to inhibition of this pathway.[1]

References

  1. Indirubin derivatives inhibit Stat3 signaling and induce apoptosis in human cancer cells. Nam, S., Buettner, R., Turkson, J., Kim, D., Cheng, J.Q., Muehlbeyer, S., Hippe, F., Vatter, S., Merz, K.H., Eisenbrand, G., Jove, R. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
 
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