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A Non-canonical Role of YAP/TEAD Is Required for Activation of Estrogen-Regulated Enhancers in Breast Cancer.

Abstract：

:YAP/TEAD are nuclear effectors of the Hippo pathway, regulating organ size and tumorigenesis largely through promoter-associated function. However, their function as enhancer regulators remains poorly understood. Through an in vivo proximity-dependent labeling (BioID) technique, we identified YAP1 and TEAD4 protein as co-regulators of ERα on enhancers. The binding of YAP1/TEAD4 to ERα-bound enhancers is augmented upon E2 stimulation and is required for the induction of E2/ERα target genes and E2-induced oncogenic cell growth. Furthermore, their enhancer binding is a prerequisite for enhancer activation marked by eRNA transcription and for the recruitment of the enhancer activation machinery component MED1. The binding of TEAD4 on active ERE-containing enhancers is independent of its DNA-binding behavior, and instead, occurs through protein-tethering trans-binding. Our data reveal a non-canonical function of YAP1 and TEAD4 as ERα cofactors in regulating cancer growth, highlighting the potential of YAP/TEAD as possible actionable drug targets for ERα+ breast cancer.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Zhu C,Li L,Zhang Z,Bi M,Wang H,Su W,Hernandez K,Liu P,Chen J,Chen M,Huang TH,Chen L,Liu Z

doi

10.1016/j.molcel.2019.06.010

subject

Has Abstract

pub_date

2019-08-22 00:00:00

pages

791-806.e8

issue

4

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(19)30443-5

journal_volume

75

pub_type

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