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TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells
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TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells
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TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells
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Journal Article
TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells
2018
Overview
Yes-associated protein (YAP), the downstream transducer of the Hippo pathway, is a key regulator of organ size, differentiation and tumorigenesis. To uncover Hippo-independent YAP regulators, we performed a genome-wide CRISPR screen that identifies the transcriptional repressor protein Trichorhinophalangeal Syndrome 1 (TRPS1) as a potent repressor of YAP-dependent transactivation. We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers. TRPS1 represses YAP-dependent function by recruiting a spectrum of corepressor complexes to joint sites. Loss of TRPS1 leads to activation of enhancers due to increased H3K27 acetylation and an altered promoter–enhancer interaction landscape.
TRPS1
is commonly amplified in breast cancer, which suggests that restrained YAP activity favours tumour growth. High TRPS1 activity is associated with decreased YAP activity and leads to decreased frequency of tumour-infiltrating immune cells. Our study uncovers TRPS1 as an epigenetic regulator of YAP activity in breast cancer.
YAP is a transcriptional co-activator downstream of Hippo pathway that displays oncogenic but also tumour suppressive functions. Here, the authors perform an unbiased genome wide CRISPR screen and identify Trichorhinophalangeal syndrome 1 (TRPS1) that represses YAP/TEAD activity independently of Hippo pathway in breast cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 45/15
/ 45/47
/ 45/91
/ Animals
/ Breast Neoplasms - metabolism
/ Cancer
/ CRISPR
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genomes
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Mice
/ Proteins
/ RNA, Small Interfering - metabolism
/ Science
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Trichorhinophalangeal syndrome
/ Tumors
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