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Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer
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  • Published: 07 February 2026

Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer

  • Spyros Tastsoglou1,2 na1,
  • Ilias V. Karagounis3 na1,
  • Marios Miliotis1,2,
  • Harika Nagandla4,
  • Kristina Diana A. Zambo4,
  • Maria Liousia3,
  • Naoto Ueno5,
  • Amit Maity3,
  • Artemis G. Hatzigeorgiou1,2 &
  • …
  • Christoforos Thomas4 

npj Breast Cancer , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Breast cancer
  • Cancer
  • Cancer genomics

Abstract

Inflammatory breast cancer (IBC) is a highly metastatic breast carcinoma, frequently characterized by estrogen receptor alpha (ERα) negativity and limited treatment options. Our previous research showed that the second ER subtype, ERβ, is associated with reduced metastasis in IBC patients and xenografts. We linked its anti-metastatic function to the inhibition of actin-based cell migration and Rho GTPase signaling. In this study, we employed a genomics approach to fully delineate the signaling underlying the anti-metastatic activity of ERβ. By cross-examining responsive mRNAs and miRNAs against chromatin binding sites in IBC cells with agonist-activated transfected and endogenous ERβ, we identified key regulatory binding motifs, direct targets, and associated biological functions. Our findings implicate pathways in development, metabolism and tumor microenvironment in the anti-metastatic action of ERβ. Clinical dataset analysis associates downstream factors with patient outcomes, indicating new molecules with therapeutic potential and highlighting the relevance of tumor repressive ERβ signaling in breast cancer.

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Data availability

RNA-seq and ChIP-seq data from KPL4 Control, ERβKO and ERβΚΟ + ERβ cells as well as Control and ERβ-expressing SUM149 cells have been uploaded into the Gene Expression Omnibus Repository (GEO) with accession numbers GSE274444 for sRNA-seq, GSE274446 for RNA-seq and GSE274448 for ChIP-seq. Analysis of data from cBioPortal (https://www.cbioportal.org/) and Metastatic Breast Cancer Project (https://mbcproject.org/data-release) utilized publicly available datasets on the respective websites. Other data that support the findings of this study are available from the corresponding author upon reasonable request. The remaining data are available within the Article, Supplementary Information or Source Data file.

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Acknowledgements

We thank Sonali Majumdar and Shashi Bala from the Genomics Core Facility at The Wistar Institute for technical assistance with the ChIP-seq and RNA-seq analysis. We also thank Jie Willey and Huiming Sun from the Morgan Welch Inflammatory Breast Cancer Research Program and Clinic at the UTMDACC for supporting the analysis of human samples. We finally thank Shaveta Kanoria for editing the manuscript.

Author information

Author notes

  1. These authors contributed equally: Spyros Tastsoglou, Ilias V. Karagounis.

Authors and Affiliations

  1. DIANA-Lab, Department of Computer Science & Biomedical Informatics, University of Thessaly, Lamia, Greece

    Spyros Tastsoglou, Marios Miliotis & Artemis G. Hatzigeorgiou

  2. Hellenic Pasteur Institute, Athens, Greece

    Spyros Tastsoglou, Marios Miliotis & Artemis G. Hatzigeorgiou

  3. Department of Radiation Oncology, School of Medicine, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA

    Ilias V. Karagounis, Maria Liousia & Amit Maity

  4. Houston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, TX, USA

    Harika Nagandla, Kristina Diana A. Zambo & Christoforos Thomas

  5. University of Hawaii Cancer Center, Honolulu, HI, USA

    Naoto Ueno

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Contributions

C.T. conceptualized the study, designed all experiments and participated in the analysis of the data. I.K., K.Z., and H.N. performed most of the experiments. A.H. supervised the analysis of the data and participated in the design of the study. S.T. and M.M. analyzed all data. C.T. wrote the manuscript. A.M. provided helpful discussions and suggestions. N.U. provided the patient data and suggestions. All authors discussed the results and commented on the manuscript.

Corresponding author

Correspondence to Christoforos Thomas.

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Competing interests

N. Ueno reports consulting roles with the following companies: AstraZeneca plc, Bayer AG, Pfizer Inc., Gilead Sciences, Inc., Chugai Pharmaceutical Co., CytoDyn Inc., Daiichi Sankyo, Inc., DynaMed, LLC, Eisai Co., Ltd., KeChow Pharma, Inc., Lavender Health Ltd., OBI Pharma Inc., OncoCyte Co., Ourotech, Inc., DBA Pear Bio, Kirilys Therapeutics, Inc., Peptilogics, Inc., Phoenix Molecular Designs, Preferred Medicine, Inc., Puma Biotechnology, Inc., Sumitomo Dainippon Pharma, Inc., Sysmex Co. Ltd., Takeda Pharmaceuticals, Ltd., Unitech Medical, Inc., CARNA Biosciences, Inc., ChemDiv, Inc., DualityBio, LARVOL, Oncolys BioPharma Inc., Rakuten Medical, Inc., Merck Co., AnHeart Therapeutics Inc., Carisma Therapeutics, Inc., Lilly, Inc. and Therimunex. He also reports speaker or preceptorship roles are held with the following companies: Bristol-Myers Squibb, CareNet Inc., Chugai Pharmaceutical Co., Genomic Health, Kyowa Hakko Kirin Co., Ltd., Sumitomo Dainippon Pharma, Inc., and Medscape. He additionally reports research agreements with the following companies: AnHeart Therapeutics Inc., Eisai Co., Ltd., Gilead Sciences, Inc., Phoenix Molecular Designs, Daiichi Sankyo, Inc., Puma Biotechnology, Inc., Merck Co., Oncolys BioPharma Inc., OBI Pharma Inc., ChemDiv, Inc., Tolero Pharmaceuticals, Inc., and VITRAC Therapeutics, LLC. outside the submitted work. C. Thomas reports grants from NIH during the conduct of the study. The other authors do not have a competing interest.

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Tastsoglou, S., Karagounis, I.V., Miliotis, M. et al. Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer. npj Breast Cancer (2026). https://doi.org/10.1038/s41523-026-00905-4

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  • Received: 05 December 2024

  • Accepted: 23 January 2026

  • Published: 07 February 2026

  • DOI: https://doi.org/10.1038/s41523-026-00905-4

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