MYC reshapes CTCF-mediated chromatin architecture in prostate cancer

Zhao Wei, Song Wang, Yaning Xu, Wenzheng Wang, Fraser Soares, Musaddeque Ahmed, Ping Su, Tingting Wang, Elias Orouji, Xin Xu, Yong Zeng, Sujun Chen, Xiaoyu Liu, Tianwei Jia, Zhaojian Liu, Lutao Du, Yunshan Wang, Shaoyong Chen, Chuanxin Wang, Housheng Hansen He () and Haiyang Guo ()
Additional contact information
Zhao Wei: Qilu Hospital of Shandong University
Song Wang: Shandong University
Yaning Xu: Shandong University
Wenzheng Wang: Shandong University
Fraser Soares: Princess Margaret Cancer Center/University Health Network
Musaddeque Ahmed: Princess Margaret Cancer Center/University Health Network
Ping Su: National Administration of Health Data
Tingting Wang: Shandong University
Elias Orouji: Epigenetics Initiative, Princess Margaret Genomics Centre
Xin Xu: Princess Margaret Cancer Center/University Health Network
Yong Zeng: Princess Margaret Cancer Center/University Health Network
Sujun Chen: Princess Margaret Cancer Center/University Health Network
Xiaoyu Liu: Shandong University
Tianwei Jia: Shandong University
Zhaojian Liu: Shandong University
Lutao Du: Shandong University
Yunshan Wang: Shandong University
Shaoyong Chen: Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School
Chuanxin Wang: Shandong University
Housheng Hansen He: Princess Margaret Cancer Center/University Health Network
Haiyang Guo: Shandong University

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract MYC is a well characterized oncogenic transcription factor in prostate cancer, and CTCF is the main architectural protein of three-dimensional genome organization. However, the functional link between the two master regulators has not been reported. In this study, we find that MYC rewires prostate cancer chromatin architecture by interacting with CTCF protein. Through combining the H3K27ac, AR and CTCF HiChIP profiles with CRISPR deletion of a CTCF site upstream of MYC gene, we show that MYC activation leads to profound changes of CTCF-mediated chromatin looping. Mechanistically, MYC colocalizes with CTCF at a subset of genomic sites, and enhances CTCF occupancy at these loci. Consequently, the CTCF-mediated chromatin looping is potentiated by MYC activation, resulting in the disruption of enhancer-promoter looping at neuroendocrine lineage plasticity genes. Collectively, our findings define the function of MYC as a CTCF co-factor in three-dimensional genome organization.

Date: 2023
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DOI: 10.1038/s41467-023-37544-3

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