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In this study, we aim at characterizing the SE landscape in breast cancer. To dissect the heterogeneity of SEs in TNBC and non-TNBC subtypes, we perform integrative transcriptomic and epigenomic analyses, and provide evidence that SEs play an important role in characterizing subtype-specific identity. We also identify corresponding targeting genes of TNBC-specific SEs, including FOXC1, MET, and ANLN. The critical function of TF FOXC1 in breast cancer growth and its clinical relevance has been determined 18, 19 . Phenotypically, overexpression of FOXC1 results in increased tumor growth and migration. However, very few studies have addressed the regulatory network of FOXC1. Here, our network biology analysis defines FOXC1 as the major node in regulating the expression of invasion and metastasis signature genes. Using CRISPR/Cas9 genomic editing, we delete the FOXC1-associated SE, and find a significant reduction of FOXC1 expression, as well as impairment of spheroid and clonogenic growth, consistent with its oncogenic properties. In addition, we identify ANLN as a TNBC-specific gene regulated by SE, contributing to TNBC tumorigenicity. Taken together, our multiomic analysis has revealed breast cancer subtype-specific SE regulatory mechanisms, and we have characterized the critical function of SEs in the specific oncogenic signaling of TNBC.
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.
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