Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors

Michael F. Ciccone, Dhivyaa Anandan, Deeptiman Chatterjee, Chen Chen, Marygrace C. Trousdell, Rebecca Anderson, Steven M. Lewis, Mackenzie K. Callaway, Chris Z. Zhao, Amritha Varshini Hanasoge Somasundara, Suzanne Russo, Shih-Ting Yang, Yixin Zhao, Julie Ostrander, John E. Wilkinson, William C. K. Pomerantz, Adam Siepel, David L. Spector, Jessica Tollkuhn and Camila O. Santos ()
Additional contact information
Michael F. Ciccone: Cold Spring Harbor Laboratory
Dhivyaa Anandan: Cold Spring Harbor Laboratory
Deeptiman Chatterjee: Cold Spring Harbor Laboratory
Chen Chen: Washington University School of Medicine in St. Louis
Marygrace C. Trousdell: Brown University
Rebecca Anderson: Cold Spring Harbor Laboratory
Steven M. Lewis: Cold Spring Harbor Laboratory
Mackenzie K. Callaway: Cold Spring Harbor Laboratory
Chris Z. Zhao: Cold Spring Harbor Laboratory
Amritha Varshini Hanasoge Somasundara: Memorial Sloan Kettering Cancer Center
Suzanne Russo: Cold Spring Harbor Laboratory
Shih-Ting Yang: Cold Spring Harbor Laboratory
Yixin Zhao: Yazhouwan National Laboratory
Julie Ostrander: University of Minnesota
John E. Wilkinson: University of Washington
William C. K. Pomerantz: University of Minnesota
Adam Siepel: Cold Spring Harbor Laboratory
David L. Spector: Cold Spring Harbor Laboratory
Jessica Tollkuhn: Cold Spring Harbor Laboratory
Camila O. Santos: Cold Spring Harbor Laboratory

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract Context-specific epigenetic dependencies, shaped by chromatin remodeling can create exploitable vulnerabilities for cancer therapies that are unique to tissue types and cellular identities. Here, we show that loss of BPTF (Bromodomain PHD Finger Transcription Factor), a core component of the NURF (Nucleosome Remodeling Factor) complex, results in the emergence of estrogen-responsive, tamoxifen-sensitive, Estrogen Receptor alpha (ERα) positive mammary tumors without altering cancer cell state and tumor pathology. Elevated ERα levels in BPTFKO mammary tumor cells are linked with decreased TGF-β activity and limited metastatic spread of mammary tumor cells to the lungs. Loss of ERα is sufficient to restore TGF-β activity and the metastatic potential in BPTFKO tumors. These findings highlight a mechanism through which BPTF regulates tumor development and progression in mammary epithelial cells, offering insights into the interplay between chromatin remodeling, estrogen signaling, and their resultant adjuvant therapeutic potential in breast cancer.

Date: 2025
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DOI: 10.1038/s41467-025-64255-8

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