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Cancers
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The Estrogen Receptor and Its Role in Cancer
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The Estrogen Receptor and Its Role in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Biomarkers".

Deadline for manuscript submissions: 15 April 2025 | Viewed by 3529

Special Issue Editors

Dr. Seth A. Wander

E-Mail Website
Guest Editor
Massachusetts General Hospital, Department of Medicine, Division of Hematology and Oncology, Boston, MA, USA
Interests: breast cancer; cancer genetics; novel and targeted therapies for breast cancer treatment
Prof. Dr. Todd W. Miller

E-Mail Website
Guest Editor
Department of Pharmacology & Toxicology and Pathology, Medical College of Wisconsin, Milwaukee, WI, USA
Interests: targeted therapies in breast cancer; anti-cancer therapeutics

Special Issue Information

Dear Colleagues,  

Estrogen-directed therapy has been the mainstay of treatment of both early-stage and metastatic breast cancer for decades. Recent genomic and molecular advances have provided new insights into the mechanisms of resistance to these commonly utilized drugs, and a variety of new agents and strategies are under active preclinical and clinical development. Expanding our understanding of the role the estrogen receptor plays in breast (and other) cancers, continuing to explore the biological basis of resistance to hormonal therapy, and developing new strategies for clinical deployment remain important priorities for the cancer research community.  

We are pleased to invite you to participate in this Special Issue, focused on the estrogen receptor and its role in cancer progression and drug resistance. This issue will be an opportunity to present articles both summarizing the tremendous progress in this area to date as well as presenting new and exciting advances in this field. We welcome articles for consideration related to basic science, translational research, and clinical studies in breast cancer (and other relevant tumor types). 

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: estrogen-related signaling in breast cancer (and other malignancies), novel insights into molecular and genomic mechanisms of resistance to hormonal therapy, new approaches to target antiestrogen resistance in breast cancer (and other malignancies) in the laboratory and clinic, and novel methodologies to image or track hormonal sensitivity.  

We look forward to receiving your contributions.

Dr. Seth A. Wander
Prof. Dr. Todd W. Miller
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • breast cancer
  • estrogen receptor
  • hormone signaling
  • therapy resistance
  • novel hormonal agents
  • antiestrogen therapy
  • selective estrogen receptor degraders
  • ESR1 mutation
  • genomic sequencing
  • precision oncology

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Published Papers (2 papers)

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Research

15 pages, 2068 KiB  
Article
The G-Protein-Coupled Estrogen Receptor Agonist G-1 Mediates Antitumor Effects by Activating Apoptosis Pathways and Regulating Migration and Invasion in Cervical Cancer Cells
by Abigail Gaxiola-Rubio, Luis Felipe Jave-Suárez, Christian David Hernández-Silva, Adrián Ramírez-de-Arellano, Julio César Villegas-Pineda, Marisa de Jesús Lizárraga-Ledesma, Moisés Ramos-Solano, Carlos Daniel Diaz-Palomera and Ana Laura Pereira-Suárez
Cancers 2024, 16(19), 3292; https://doi.org/10.3390/cancers16193292 - 27 Sep 2024
Viewed by 696
Abstract
Background/Objectives: Estrogens and HPV are necessary for cervical cancer (CC) development. The levels of the G protein-coupled estrogen receptor (GPER) increase as CC progresses, and HPV oncoproteins promote GPER expression. The role of this receptor is controversial due to its anti- and pro-tumor [...] Read more.
Background/Objectives: Estrogens and HPV are necessary for cervical cancer (CC) development. The levels of the G protein-coupled estrogen receptor (GPER) increase as CC progresses, and HPV oncoproteins promote GPER expression. The role of this receptor is controversial due to its anti- and pro-tumor effects. This study aimed to determine the effect of GPER activation, using its agonist G-1, on the transcriptome, cell migration, and invasion in SiHa cells and non-tumorigenic keratinocytes transduced with the HPV16 E6 or E7 oncogenes. Methods: Transcriptome analysis was performed to identify G-1-enriched pathways in SiHa cells. We evaluated cell migration, invasion, and the expression of associated proteins in SiHa, HaCaT-16E6, and HaCaT-16E7 cells using various assays. Results: Transcriptome analysis revealed pathways associated with proliferation/apoptosis (TNF-α signaling, UV radiation response, mitotic spindle formation, G2/M cell cycle, UPR, and IL-6/JAK/STAT), cellular metabolism (oxidative phosphorylation), and cell migration (angiogenesis, EMT, and TGF-α signaling) in SiHa cells. Key differentially expressed genes included PTGS2 (pro/antitumor), FOSL1, TNFRSF9, IL1B, DIO2, and PHLDA1 (antitumor), along with under-expressed genes with pro-tumor effects that may inhibit proliferation. Additionally, DKK1 overexpression suggested inhibition of cell migration. G-1 increased vimentin expression in SiHa cells and reduced it in HaCaT-16E6 and HaCaT-16E7 cells. However, G-1 did not affect α-SMA expression or cell migration in any of the cell lines but increased invasion in HaCaT-16E7 cells. Conclusions: GPER is a promising prognostic marker due to its ability to activate apoptosis and inhibit proliferation without promoting migration/invasion in CC cells. G-1 could potentially be a tool in the treatment of this neoplasia. Full article
(This article belongs to the Special Issue The Estrogen Receptor and Its Role in Cancer)
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16 pages, 2979 KiB  
Article
TRIM33 Is a Co-Regulator of Estrogen Receptor Alpha
by Bianca A. Romo, Barbara Karakyriakou, Lauren Cressey, Brooke L. Brauer, Huijuan Yang, Alexa Warren, Anneka L. Johnson, Arminja N. Kettenbach and Todd W. Miller
Cancers 2024, 16(5), 845; https://doi.org/10.3390/cancers16050845 - 20 Feb 2024
Viewed by 2424
Abstract
Estrogen receptor alpha (ER)-positive breast cancer is responsible for over 60% of breast cancer cases in the U.S. Among patients diagnosed with early-stage ER+ disease, 1/3 will experience recurrence despite treatment with adjuvant endocrine therapy. ER is a nuclear hormone receptor responsible for [...] Read more.
Estrogen receptor alpha (ER)-positive breast cancer is responsible for over 60% of breast cancer cases in the U.S. Among patients diagnosed with early-stage ER+ disease, 1/3 will experience recurrence despite treatment with adjuvant endocrine therapy. ER is a nuclear hormone receptor responsible for estrogen-driven tumor growth. ER transcriptional activity is modulated by interactions with coregulators. Dysregulation of the levels of these coregulators is involved in the development of endocrine resistance. To identify ER interactors that modulate transcriptional activity in breast cancer, we utilized biotin ligase proximity profiling of ER interactomes. Mass spectrometry analysis revealed tripartite motif containing 33 (TRIM33) as an estrogen-dependent interactor of ER. shRNA knockdown showed that TRIM33 promoted ER transcriptional activity and estrogen-induced cell growth. Despite its known role as an E3 ubiquitin ligase, TRIM33 increased the stability of endogenous ER in breast cancer cells. TRIM33 offers a novel target for inhibiting estrogen-induced cancer cell growth, particularly in cases of endocrine resistance driven by ER (ESR1) gene amplification or overexpression. Full article
(This article belongs to the Special Issue The Estrogen Receptor and Its Role in Cancer)
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