TGIF调控一个前馈网络，该网络增强Wnt信号传导以驱动乳腺肿瘤发生。
TGIF governs a feed-forward network that empowers Wnt signaling to drive mammary tumorigenesis.
作者信息
Zhang Ming-Zhu, Ferrigno Olivier, Wang Zhe, Ohnishi Mutsuko, Prunier Céline, Levy Laurence, Razzaque Mohammed, Horne Williams C, Romero Damian, Tzivion Guri, Colland Frédéric, Baron Roland, Atfi Azeddine
机构信息
Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA; Department of Orthopaedics, Tongji University School of Medicine, Shanghai 200065, China.
Laboratory of Cell Signaling and Carcinogenesis, INSERM UMRS938, 184 Rue du Faubourg St-Antoine, 75571 Paris, France.
出版信息
Cancer Cell. 2015 Apr 13;27(4):547-60. doi: 10.1016/j.ccell.2015.03.002.
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.
摘要
许多具有Wnt信号超激活的人类癌症类型在该信号通路的已知效应器中未显示出致病性改变。在此，我们报告了TGIF在Wnt信号通路中的功能。TGIF与β-连环蛋白破坏复合物中的Axin1和Axin2结合并使其转向，从而使β-连环蛋白积累。有趣的是，Wnt信号通路的激活诱导了TGIF的表达，这揭示了一个前馈环，可确保Wnt信号通路的有效整合。在三阴性乳腺癌（TNBC）中，TGIF水平升高与高Wnt信号通路及患者的不良生存率相关。此外，基因实验表明，Tgif1基因敲除阻碍了MMTV-Wnt1小鼠的乳腺肿瘤发展，进一步强调了TGIF对致癌性Wnt信号通路的需求。
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