Research ArticleCancer Biology

Partial inhibition of gp130-Jak-Stat3 signaling prevents Wnt–β-catenin–mediated intestinal tumor growth and regeneration

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Science Signaling  30 Sep 2014:
Vol. 7, Issue 345, pp. ra92
DOI: 10.1126/scisignal.2005411

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A Novel Strategy for Treating Colon Cancer

In most patients, colon cancer arises from a mutation in the gene encoding APC, which results in constitutive activation of the β-catenin pathway. Inhibition of this pathway interferes with the continuous renewal of the epithelial cells that line the intestinal tract and therefore may confer only limited therapeutic benefit. Phesse et al. discovered that the signaling pathway involving the receptor gp130, the associated Jak kinases, and the transcription factor Stat3 enhanced the growth of intestinal tumors in mice. Conversely, genetic or pharmacological inhibition of this pathway reduced tumor growth by increasing the expression of genes encoding the p21 and p16 proteins that halt cell division, through a cell-intrinsic mechanism. Thus, drugs targeting the Jak-Stat3 pathway, which are currently in clinical trials for the treatment of hematological malignancies, may also be useful for treating colon cancer.

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