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Targeting Tryptophan Catabolism: A Novel Method to Block Triple-Negative Breast Cancer Metastasis

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Technical Report,01 Apr 2015,31 Mar 2016

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University of Colorado Aurora United States

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Triple negative breast cancer TNBC cells strongly upregulate two related pathways, the kynurenine pathway KP in forced suspension culture. The KP is the principal route of tryptophan catabolism. Interestingly, the intermediate tryptophan metabolite kynurenine Kyn was recently identified as an endogenous ligand for AhR, a transcription factor that was also upregulated in suspension. Kyn activation of AhR promotes motility of glioma cells, and increased AhR expression and activity was found to be a characteristic of human and mouse mammary tumors. AhR is also in many immune cell types and its activation decreases T-cell activity leading to tumor immune escape. Since the rate limiting enzyme TDO2 increases in TNBC, the goal of our proposal is to determine if we can target this pathway that helps TNBC metastasize. Our hypothesis is that upregulation of kynurenine by TNBC facilitates survival in transit to metastatic sites and immune suppression and thereby mediates the highly metastatic nature of this subtype. We now have one published work and work in progress suggests that this hypothesis holds true.

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