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Endocrines
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Molecular Mechanisms of Estrogen Signaling Pathways
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Molecular Mechanisms of Estrogen Signaling Pathways

A special issue of Endocrines (ISSN 2673-396X).

Deadline for manuscript submissions: closed (20 May 2021) | Viewed by 9887

Special Issue Editors

Dr. Muriel Le Romancer

E-Mail Website
Guest Editor
Inserm U1052, Centre de Recherche en Cancérologie de Lyon (CRCL), Lyon, France
Interests: breast cancer; estrogen receptor; progesterone receptor; cell signaling; arginine methylation; arginine demethylation; post translational modifications; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals
Dr. Coralie Poulard

E-Mail Website
Guest Editor
Inserm U1052, Centre de Recherche en Cancérologie de Lyon (CRCL), Lyon, France
Interests: steroid hormone receptor; breast cancer; protein methylation; coregulators

Special Issue Information

Dear Colleagues,

The steroid hormone estrogen plays a critical role in numerous target tissues including the reproductive tract, the nervous, vascular and skeletal systems. Its pleiotropic effects are mediated mainly by two receptors, estrogen receptor alpha (ERα) and beta (ERβ), members of the nuclear receptors family, which function as ligand-dependent transcription factors. More recently, isoforms of ERα have been identified (ERα46, ERα36) displaying different mechanisms of action and adding a level of complexity in the integration of estrogen biological effects. Estrogen signaling is highly complex as besides its classical genomic action, a non genomic pathway involving protein kinases also takes place. Moreover, interference with growth factors signaling participates in the integration of various external signals.

In addition, estrogen receptors signaling involves the recruitment of a large number of coregulators, which participates in the diversity and the specificity of biological responses. These receptors are also highly modified by post translational modifications (PTMs), such as phosphorylation, methylation and acetylation involved in the fine tuning of their activities. The complexity of ER regulation is a rapidly growing issue as new coregulators and PTMs are continuously identified. Moreover, ER is also able to interact with other members of the steroid hormone receptors family as with the progesterone receptor (PR) or the glucocorticoid receptor (GR) modulating estrogen signaling.

Understanding deeply the molecular mechanisms of estrogen signaling is an important challenge as estrogen is involved in pathology such as breast and endometrial cancers, but also to better understand how endocrine disruptors interfere with these pathways. 

This special issue of Endocrines welcomes in vitro and in vivo studies as well as comprehensive reviews on estrogen molecular mechanisms, diagnostic and therapeutic advances in treatment of pathologies involving estrogens.

Dr. Muriel Le Romancer
Dr. Coralie Poulard
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Endocrines is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Estrogen 
  • Estrogen receptors 
  • Genomic signaling 
  • Non genomic signaling 
  • Coregulators 
  • Post translational modifications 
  • ER isoforms 
  • Cancer

Published Papers (3 papers)

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10 pages, 1455 KiB  
Review
ERβ in Triple-Negative Breast Cancer: Emerging Concepts and Therapeutic Possibilities
by Alessandra Monaco, Fabrizio Licitra, Martina Di Gisi, Giovanni Galasso, Marzia Di Donato, Pia Giovannelli, Antimo Migliaccio and Gabriella Castoria
Endocrines 2021, 2(3), 356-365; https://doi.org/10.3390/endocrines2030033 - 13 Sep 2021
Cited by 7 | Viewed by 3233
Abstract
Despite the improvements in diagnostic and therapeutic approaches, breast cancer still remains one of the world’s leading causes of death among women. Particularly, triple negative breast cancer (TNBC) is characterized by aggressiveness, metastatic spreading, drug resistance and a very high percentage of death [...] Read more.
Despite the improvements in diagnostic and therapeutic approaches, breast cancer still remains one of the world’s leading causes of death among women. Particularly, triple negative breast cancer (TNBC) is characterized by aggressiveness, metastatic spreading, drug resistance and a very high percentage of death in patients. Nowadays, identification of new targets in TNBC appears very compelling. TNBC are considered negative for the estrogen receptor alpha (ERα) expression. Nevertheless, they often express ERβ and its variants. As such, this TNBC subtype still responds to estrogens. While the ERβ1 variant seems to act as a tumor-suppressor, the two variants ERβ2 and 5 exhibit pro-oncogenic activities in TNBC. Thus, ERβ1 activation might be used to limit the growth and spreading as well as to increase the drug sensitivity of TNBC. In contrast, the pro-oncogenic properties of ERβ2 and ERβ5 suggest the possible development and clinical use of specific antagonists in TNBC treatment. Furthermore, the role of ERβ might be regarded in the context of the androgen receptor (AR) expression, which represents another key marker in TNBC. The relationship between AR and ERβ as well as the ability to modulate the receptor-mediated effects through agonists/antagonists represent a challenge to develop more appropriate therapies in clinical management of TNBC patients. In this review, we will discuss the most recent data in the field. Therapeutic implications of these findings are also presented in the light of the discovery of specific ERβ modulators. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Estrogen Signaling Pathways)
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14 pages, 1775 KiB  
Review
Pathological Maintenance and Evolution of Breast Cancer: The Convergence of Irreversible Biological Actions of ER Alpha
by Guy Leclercq
Endocrines 2021, 2(1), 1-14; https://doi.org/10.3390/endocrines2010001 - 24 Dec 2020
Cited by 1 | Viewed by 3278
Abstract
Estrogen receptor alpha (ERα) is a modulator of breast cancer maintenance and evolution. Hence, analysis of underlying mechanisms by which ERα operates is of importance for the improvement of the hormonal therapy of the disease. This review focuses on the irreversible character of [...] Read more.
Estrogen receptor alpha (ERα) is a modulator of breast cancer maintenance and evolution. Hence, analysis of underlying mechanisms by which ERα operates is of importance for the improvement of the hormonal therapy of the disease. This review focuses on the irreversible character of the mechanism of action of ERα, which also concerns other members of the steroid hormones receptors family. ERα moves in permanence between targets localized especially at the chromatin level to accomplish gene transcriptions imposed by the estrogenic ligands and specific antagonists. Receptor association as at the plasma membrane, where it interacts with other recruitment sites, extends its regulatory potency to growth factors and related peptides through activation of signal transductions pathways. If the latter procedure is suitable for the transcriptions in which the receptor operates as a coregulator of another transcription factor, it is of marginal influence with regard to the direct estrogenic regulation procedure, especially in the context of the present review. Irreversibility of the successive steps of the underlying transcription cycle guarantees maintenance of homeostasis and evolution according to vital necessities. To justify this statement, reported data are essentially described in a holistic view rather than in the context of exhaustive analysis of a molecular event contributing to a specific function as well as in a complementary perspective to elaborate new therapeutic approaches with antagonistic potencies against those tumors promoting ERα properties. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Estrogen Signaling Pathways)
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11 pages, 3916 KiB  
Brief Report
Real-Time Challenging of ERα Y537S Mutant Transcriptional Activity in Living Cells
by Manuela Cipolletti, Sara Pescatori and Filippo Acconcia
Endocrines 2021, 2(1), 54-64; https://doi.org/10.3390/endocrines2010006 - 10 Mar 2021
Cited by 5 | Viewed by 2657
Abstract
Metastatic estrogen receptor α (ERα)-expressing breast cancer (BC) occurs after prolonged patient treatment with endocrine therapy (ET) (e.g., aromatase inhibitors—AI; 4OH-tamoxifen—4OH-Tam). Often these metastatic BCs express a mutated ERα variant (e.g., Y537S), which is transcriptionally hyperactive, sustains uncontrolled proliferation, and renders tumor cells [...] Read more.
Metastatic estrogen receptor α (ERα)-expressing breast cancer (BC) occurs after prolonged patient treatment with endocrine therapy (ET) (e.g., aromatase inhibitors—AI; 4OH-tamoxifen—4OH-Tam). Often these metastatic BCs express a mutated ERα variant (e.g., Y537S), which is transcriptionally hyperactive, sustains uncontrolled proliferation, and renders tumor cells insensitive to ET drugs. Therefore, new molecules blocking hyperactive Y537S ERα mutation transcriptional activity are requested. Here we generated an MCF-7 cell line expressing the Y537S ERα mutation stably expressing an estrogen-responsive element (ERE) promoter, which activity can be monitored in living cells. Characterization of this cell line shows both hyperactive basal transcriptional activity with respect to normal MCF-7 cells, which stably express the same ERE-based promoter and a decreased effect of selective ER downregulators (SERDs) in reducing Y537S ERα mutant transcriptional activity with respect to wild type ERα transcriptional activity. Kinetic profiles of Y537S ERα mutant-based transcription produced by both drugs inducing receptor degradation and siRNA-mediated depletion of specific proteins (e.g., FOXA1 and caveolin1) reveals biphasic dynamics of the inhibition of the receptor-regulated transcriptional effects. Overall, we report a new model where to study the behavior of the Y537S ERα mutant that can be used for the identification of new targets and pathways regulating the Y537S ERα transcriptional activity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Estrogen Signaling Pathways)
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