CRISPR Screening of Transcribed Super-Enhancers Identifies Drivers of Triple-Negative Breast Cancer Progression
Triple-negative breast cancer (TNBC) is the most therapeutically recalcitrant form of breast cancer, which is due in part to the paucity of targeted therapies. A systematic analysis of regulatory elements that extend beyond protein-coding genes could uncover avenues for therapeutic intervention. To this end, we analyzed the regulatory mechanisms of TNBC-specific transcriptional enhancers together with their noncoding enhancer RNA (eRNA) transcripts. The functions of the top 30 eRNA-producing super-enhancers were systematically probed using high-throughput CRISPR-interference assays coupled to RNA sequencing that enabled unbiased detection of target genes genome-wide. Generation of high-resolution Hi-C chromatin interaction maps enabled annotation of the direct target genes for each super-enhancer, which highlighted their proclivity for genes that portend worse clinical outcomes in patients with TNBC. Illustrating the utility of this dataset, deletion of an identified super-enhancer controlling the nearby PODXL gene or specific degradation of its eRNAs led to profound inhibitory effects on target gene expression, cell proliferation, and migration. Furthermore, loss of this super-enhancer suppressed tumor growth and metastasis in TNBC mouse xenograft models. Single-cell RNA sequencing and assay for transposase-accessible chromatin with high-throughput sequencing analyses demonstrated the enhanced activity of this super-enhancer within the malignant cells of TNBC tumor specimens compared with nonmalignant cell types. Collectively, this work examines several fundamental questions about how regulatory information encoded into eRNA-producing super-enhancers drives gene expression networks that underlie the biology of TNBC. Significance: Integrative analysis of eRNA-producing super-enhancers defines molecular mechanisms controlling global patterns of gene expression that regulate clinical outcomes in breast cancer, highlighting the potential of enhancers as biomarkers and therapeutic targets.
Authors
- Douglas H. Phanstiel (ORCID: https://orcid.org/0000-0003-2123-0051)
- Eric S. Davis (ORCID: https://orcid.org/0000-0003-4051-3217)
- Matthew J. Regner (ORCID: https://orcid.org/0000-0001-9838-568X)
- Caitlin M. King (ORCID: https://orcid.org/0000-0001-6305-9331)
- Kamila Wiśniewska (ORCID: https://orcid.org/0000-0002-6388-7265)
- Alisha R. Coffey (ORCID: https://orcid.org/0000-0003-1792-7999)
- Michael R. Kelly (ORCID: https://orcid.org/0000-0003-4642-0118)
- Hector L. Franco (ORCID: https://orcid.org/0000-0001-9354-0679)
- Raúl Méndez-Giráldez (ORCID: https://orcid.org/0000-0003-1853-9429)
- Michael W. Lewis (ORCID: https://orcid.org/0000-0002-8649-6689)
Institutions
- University of North Carolina at Chapel Hill (US)
- University of Puerto Rico System (PR)
- Clinical Research Puerto Rico (PR)
Publication Details
- Journal
- Cancer Research
- Published
- 2024-08-26
- DOI
- https://doi.org/10.1158/0008-5472.can-23-3995
- Citations
- 12
- Primary Topic
- Genomics and Chromatin Dynamics
- Type
- article
- Field-Weighted Citation Impact
- 2.81
Funders
- U.S. Department of Defense
- American Cancer Society
- Breast Cancer Research Foundation
- Susan G. Komen
- National Institutes of Health
- National Cancer Institute
- Congressionally Directed Medical Research Programs