The transcriptional co-activators YAP and AIB1 individually promote breast cancer progression, but are not known to be mechanistically linked. A study published in this issue of EMBO Reports [1] now shows that YAP-AIB1 form a physical complex in breast epithelial cells that cooperates in both activation and, unexpectedly, repression of key breast cancer genes. The repressive effect is due to the recruitment of ANCO1, a previously defined AIB1 interactor [2] that binds and inhibits the YAP-AIB1 complex. These data identify ANCO1 as a candidate tumor suppressor through YAP-AIB1 inhibition and could hint at a broader crosstalk between pathways that utilize YAP and AIB1 to control epithelial homeostasis.

中文翻译：

---

一个压制者将它们全部统治：ANCO1链接YAP和AIB1。

转录共激活因子YAP和AIB1分别促进乳腺癌的进展，但在机理上未知。现在，本期《 EMBO报告》 [1]上发表的一项研究表明，YAP-AIB1在乳腺癌上皮细胞中形成一种物理复合物，在激活和意外抑制关键乳腺癌基因方面均发挥了作用。抑制作用是由于ANCO1的募集，ANCO1是先前定义的AIB1相互作用物[2]，可结合并抑制YAP-AIB1复合物。这些数据通过抑制YAP-AIB1将ANCO1识别为候选肿瘤抑制物，并可能暗示利用YAP和AIB1控制上皮稳态的途径之间存在更广泛的串扰。