| Literature DB >> 25873176 |
Ming-Zhu Zhang1, Olivier Ferrigno2, Zhe Wang3, Mutsuko Ohnishi4, Céline Prunier2, Laurence Levy2, Mohammed Razzaque4, Williams C Horne4, Damian Romero3, Guri Tzivion3, Frédéric Colland5, Roland Baron4, Azeddine Atfi6.
Abstract
Many types of human cancers having hyperactivated Wnt signaling display no causative alterations in known effectors of this pathway. Here, we report a function of TGIF in Wnt signaling. TGIF associates with and diverts Axin1 and Axin2 from the β-catenin destruction complex, therefore allowing β-catenin accrual. Intriguingly, activation of Wnt signaling induces the expression of TGIF, which unveils a feed-forward loop that ensures effective integration of Wnt signaling. In triple-negative breast cancers (TNBC), elevated levels of TGIF correlate with high Wnt signaling and poor survival of patients. Moreover, genetic experiments revealed that Tgif1 ablation impeded mammary tumor development in MMTV-Wnt1 mice, further underscoring a requirement of TGIF for oncogenic Wnt signaling.Entities:
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Year: 2015 PMID： 25873176 PMCID： PMC4398914 DOI： 10.1016/j.ccell.2015.03.002
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743