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首页> 外文期刊>Cancer Cell >DACT3 is an epigenetic regulator of Wnt/beta-catenin signaling in colorectal cancer and is a therapeutic target of histone modifications.
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DACT3 is an epigenetic regulator of Wnt/beta-catenin signaling in colorectal cancer and is a therapeutic target of histone modifications.

机译：DACT3是结直肠癌中Wnt /β-catenin信号传导的表观遗传调节剂，是组蛋白修饰的治疗靶标。

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摘要

Genetic and epigenetic defects in Wnt/beta-catenin signaling play important roles in colorectal cancer progression. Here we identify DACT3, a member of the DACT (Dpr/Frodo) gene family, as a negative regulator of Wnt/beta-catenin signaling that is transcriptionally repressed in colorectal cancer. Unlike other Wnt signaling inhibitors that are silenced by DNA methylation, DACT3 repression is associated with bivalent histone modifications. Remarkably, DACT3 expression can be robustly derepressed by a pharmacological combination that simultaneously targets both histone methylation and deacetylation, leading to strong inhibition of Dishevelled (Dvl)-mediated Wnt/beta-catenin signaling and massive apoptosis of colorectal cancer cells. Our study identifies DACT3 as an important regulator of Wnt/beta-catenin signaling in colorectal cancer and suggests a potential strategy for therapeutic control of Wnt/beta-catenin signaling in colorectal cancer.
机译：Wnt /β-catenin信号传导的遗传和表观遗传缺陷在结直肠癌的进展中起重要作用。在这里，我们确定DACT3（DACT（Dpr / Frodo）基因家族的成员）是Wnt /β-catenin信号转导在结直肠癌中被抑制的负调控因子。与其他通过DNA甲基化沉默的Wnt信号抑制剂不同，DACT3抑制与二价组蛋白修饰有关。值得注意的是，DACT3的表达可被同时靶向组蛋白甲基化和去乙酰化的药理学组合强烈抑制，从而导致对Disheveled（Dvl）介导的Wnt /β-catenin信号的强烈抑制和结直肠癌细胞的大量凋亡。我们的研究确定DACT3是大肠癌Wnt /β-catenin信号传导的重要调节剂，并提出了治疗性控制Wnt /β-catenin信号在大肠癌中的潜在策略。

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