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Berman AY, Manna S, Schwartz NS, et al. ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism. Signal Transduct Target Ther. 2017;2doi: 10.1038/sigtrans.2017.35.
Berman, A. Y., Manna, S., Schwartz, N. S., Katz, Y. E., Sun, Y., Behrmann, C. A., Yu, J. J., Plas, D. R., Alayev, A., & Holz, M. K. (2017). ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism. Signal transduction and targeted therapy, 2. https://doi.org/10.1038/sigtrans.2017.35
Berman, Adi Y, et al. "ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism." Signal transduction and targeted therapy vol. 2 (2017). doi: https://doi.org/10.1038/sigtrans.2017.35
Berman AY, Manna S, Schwartz NS, Katz YE, Sun Y, Behrmann CA, Yu JJ, Plas DR, Alayev A, Holz MK. ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism. Signal Transduct Target Ther. 2017;2. doi: 10.1038/sigtrans.2017.35. Epub 2017 Aug 25. PMID: 28890840; PMCID: PMC5589335.
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Signal Transduct Target Ther. 2017;2. doi: 10.1038/sigtrans.2017.35. Epub 2017 Aug 25.

ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism.

Signal transduction and targeted therapy

Adi Y Berman, Subrata Manna, Naomi S Schwartz, Yardena E Katz, Yang Sun, Catherine A Behrmann, Jane J Yu, David R Plas, Anya Alayev, Marina K Holz

Affiliations

  1. Department of Biology, Yeshiva University, New York, NY, USA.
  2. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
  3. Department of Cancer Biology; University of Cincinnati, Cincinnati, OH, USA.
  4. Department of Molecular Pharmacology and the Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY, USA.

PMID: 28890840 PMCID: PMC5589335 DOI: 10.1038/sigtrans.2017.35

Abstract

Estrogen-related receptor alpha (ERRα) is an orphan nuclear factor that is a master regulator of cellular energy metabolism. ERRα is overexpressed in a variety of tumors, including ovarian, prostate, colorectal, cervical and breast, and is associated with a more aggressive tumor and a worse outcome. In breast cancer, specifically, high ERRα expression is associated with an increased rate of recurrence and a poor prognosis. Because of the common functions of ERRα and the mTORC1/S6K1 signaling pathway in regulation of cellular metabolism and breast cancer pathogenesis, we focused on investigating the biochemical relationship between ERRα and S6K1. We found that ERRα negatively regulates S6K1 expression by directly binding to its promoter. Downregulation of ERRα expression sensitized ERα-negative breast cancer cells to mTORC1/S6K1 inhibitors. Therefore, our results show that combinatorial inhibition of ERRα and mTORC1/S6K1 may have clinical utility in treatment of triple-negative breast cancer, and warrants further investigation.

Conflict of interest statement

COMPETING INTERESTS The authors declare no conflict of interest.

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