Reviewers Comments
Reviewers Comments
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DOI：
10.5194/angeo-2018-92-rc2
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发表时间：
2018-10
期刊：
影响因子：
--
通讯作者：
Anonymous
中科院分区：
文献类型：
--
作者：
Anonymous
在题为“Targeting EZH 2 reactivates a breast cancer subtype-specific antimetastatic transcriptional program”的手稿中，作者证明了EZH 2的遗传或药理学靶向在小鼠模型和PDX模型中抑制Luminal B乳腺癌转移。从机制上讲，EZH 2的消融通过消除H3 K27 me 3沉积来重新激活FOXC 1，然后FOXC 1驱动一组抗转移基因的表达。他们进一步发现，较高的FOXC 1水平可预测Luminal B乳腺癌患者的良好结局，并表明FOXC 1可作为Luminal-B亚型乳腺癌的有希望的治疗靶点。尽管该手稿描述了关于EZH 2：FOXC 1轴在乳腺癌的luminal-B亚型中的类型特异性作用的有趣发现，但仍有几个主要问题需要解决。
In the manuscript entitled “Targeting EZH2 reactivates a breast cancer subtype-specific antimetastatic transcriptional program”, the authors demonstrated that genetic or pharmacological targeting of the Ezh2 inhibits Luminal B breast cancer metastasis in both mouse model and PDX model. Mechanistically, ablation of EZH2 reactivates FOXC1 by elimination of H3K27me3 deposition then FOXC1 drives expression of a panel of anti-metastasis genes. They further found that higher FOXC1 levels are predictive of favorable outcome specifically in Luminal B breast cancer patients and suggested that FOXC1 could serve as a promising therapeutic target for luminal-B subtype breast cancer. Although the manuscript describes interesting findings about the type specific role of EZH2:FOXC1 axis in luminal-B subtype of breast cancer, there are several major concerns that need to be addressed.