Department for BioMedical Research, University of Bern, Switzerland.
Department for BioMedical Research, University of Bern, Switzerland; Bern Center for Precision Medicine, University of Bern and Inselspital, Bern, Switzerland.
Cancer Cell. 2020 Sep 14;38(3):309-311. doi: 10.1016/j.ccell.2020.08.009.
An outgrowth of therapy-resistant prostate cancers (PCa) with enhanced metastatic potential may be triggered by inhibitors of androgen receptor (AR) signaling, often via epigenetic rewiring. In this issue of Cancer Cell, Yuan et al. demonstrate how SETD2 integrates EZH2 and AMPK signaling pathways to keep PCa metastasis in check.
治疗抵抗性前列腺癌（PCa）的生长可能会受到雄激素受体（AR）信号抑制剂的触发，这种抑制剂通常通过表观遗传重排来增强转移潜能。在本期《癌细胞》杂志中，Yuan 等人展示了 SETD2 如何整合 EZH2 和 AMPK 信号通路来抑制 PCa 的转移。
