Nature communications · 2025
Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.
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Ciccone Michael F, Anandan Dhivyaa, Chatterjee Deeptiman, Chen Chen, Trousdell Marygrace C, Anderson Rebecca, Lewis Steven M, Callaway Mackenzie K, Zhao Chris Z, Hanasoge Somasundara Amritha Varshini, Russo Suzanne, Yang Shih-Ting, Zhao Yixin, Ostrander Julie, Wilkinson John E, Pomerantz William C K, Siepel Adam, Spector David L, Tollkuhn Jessica, Dos Santos Camila O
Аннотация
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.