Defining super-enhancer landscape in triple-negative breast cancer by multiomic profiling

Hao Huang, Jianyang Hu, Alishba Maryam, Qinghua Huang, Yuchen Zhang, Saravanan Ramakrishnan, Jingyu Li, Haiying Ma, Victor W. S. Ma, Wah Cheuk, Grace Y. K. So, Wei Wang, William C. S. Cho, Liang Zhang, Kui Ming Chan, Xin Wang () and Y. Rebecca Chin ()
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Hao Huang: City University of Hong Kong
Jianyang Hu: City University of Hong Kong
Alishba Maryam: City University of Hong Kong
Qinghua Huang: Guangxi Medical University
Yuchen Zhang: City University of Hong Kong
Saravanan Ramakrishnan: City University of Hong Kong
Jingyu Li: City University of Hong Kong
Haiying Ma: City University of Hong Kong
Victor W. S. Ma: Queen Elizabeth Hospital
Wah Cheuk: Queen Elizabeth Hospital
Grace Y. K. So: Queen Elizabeth Hospital
Wei Wang: City University of Hong Kong
William C. S. Cho: Queen Elizabeth Hospital
Liang Zhang: City University of Hong Kong
Kui Ming Chan: City University of Hong Kong
Xin Wang: City University of Hong Kong
Y. Rebecca Chin: City University of Hong Kong

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: Abstract Breast cancer is a heterogeneous disease, affecting over 3.5 million women worldwide, yet the functional role of cis-regulatory elements including super-enhancers in different breast cancer subtypes remains poorly characterized. Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor prognosis. Here we apply integrated epigenomic and transcriptomic profiling to uncover super-enhancer heterogeneity between breast cancer subtypes, and provide clinically relevant biological insights towards TNBC. Using CRISPR/Cas9-mediated gene editing, we identify genes that are specifically regulated by TNBC-specific super-enhancers, including FOXC1 and MET, thereby unveiling a mechanism for specific overexpression of the key oncogenes in TNBC. We also identify ANLN as a TNBC-specific gene regulated by super-enhancer. Our studies reveal a TNBC-specific epigenomic landscape, contributing to the dysregulated oncogene expression in breast tumorigenesis.

Date: 2021
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DOI: 10.1038/s41467-021-22445-0

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