Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and...
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 4544

Special Issue Editor

Dr. Laura Muñoz-Moreno

E-Mail Website
Guest Editor
Departamento de Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud, Universidad de Alcalá, Campus Universitario, Crtra A2, Km. 33,600, 28805 Alcalá de Henares, Spain
Interests: GHRH; epithelial–mesenchymal transition; prostate cancer; breast cancer; tumor progression; exosomes; angiogenesis; antagonists; cell adhesion; cell proliferation

Special Issue Information

Dear Colleagues,

Understanding the role of hormonal receptors in cancer is paramount for developing effective treatment strategies. Hormonal receptors, such as estrogen and progesterone receptors in breast cancer, play crucial roles in tumor growth and progression. They orchestrate gene expression, fostering cellular proliferation and survival upon activation by their corresponding hormones. In cancers sensitive to hormonal cues, aberrant receptor signaling precipitates unchecked cellular proliferation, thereby fueling tumorigenesis. The molecular mechanisms underlying hormonal receptor activity in cancer involve complex signaling pathways and interactions with other cellular components. The dysregulation of these pathways can lead to resistance to conventional therapies and disease progression. Thus, targeted therapies that specifically inhibit hormonal receptor signaling have emerged as promising treatment options. Various strategies have been devised to target hormonal receptors in cancer. These include hormone receptor antagonists, which block receptor activation, and inhibitors of downstream signaling pathways involved in receptor-mediated tumorigenesis.

Therefore, the aim of this Special Issue, titled “The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies”, is to provide novel insights into the molecular action of hormone receptors and new targeted therapies for human cancer. Contributions on these related topics are welcomed, including original research and reviews.

Dr. Laura Muñoz-Moreno
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • hormone receptors
  • cancer
  • cell signaling
  • cancer therapeutics
  • cancer proliferation
  • hormone-sensitive cancers

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

18 pages, 3176 KiB  
Article
Antagonist of Growth Hormone-Releasing Hormone Receptor MIA-690 Suppresses the Growth of Androgen-Independent Prostate Cancers
by Laura Muñoz-Moreno, M. Isabel Gómez-Calcerrada, M. Isabel Arenas, M. José Carmena, Juan C. Prieto, Andrew V. Schally and Ana M. Bajo
Int. J. Mol. Sci. 2024, 25(20), 11200; https://doi.org/10.3390/ijms252011200 - 18 Oct 2024
Viewed by 681
Abstract
The development of resistance remains the primary challenge in treating castration-resistant prostate cancer (CRPC). GHRH receptors (GHRH-R), which are coupled to G-proteins (GPCRs), can mediate EGFR transactivation, offering an alternative pathway for tumour survival. This study aimed to evaluate the effects of the [...] Read more.
The development of resistance remains the primary challenge in treating castration-resistant prostate cancer (CRPC). GHRH receptors (GHRH-R), which are coupled to G-proteins (GPCRs), can mediate EGFR transactivation, offering an alternative pathway for tumour survival. This study aimed to evaluate the effects of the GHRH-R antagonist MIA-690, in combination with the EGFR inhibitor Gefitinib, on cell viability, adhesion, gelatinolytic activity, and the cell cycle in advanced prostate cancer PC-3 cells. The findings demonstrate a synergistic effect between MIA-690 and Gefitinib, leading to the inhibition of cell viability, adhesion, and metalloprotease activity. Cell cycle analysis suggests that both compounds induce cell cycle arrest, both individually and in combination. Furthermore, similar effects of the GHRH-R antagonist MIA-690 combined with Gefitinib were observed in PC-3 tumours developed by subcutaneous injection in athymic nude mice 36 days post-inoculation. These results indicate that combined therapy with a GHRH-R antagonist and an EGFR inhibitor exerts a stronger antitumor effect compared to monotherapy by preventing transactivation between EGFR and GHRH-R in CRPC. Full article
(This article belongs to the Special Issue The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies)
►▼ Show Figures

Figure 1

13 pages, 5318 KiB  
Article
The GPR30 Receptor Is Involved in IL-6-Induced Metastatic Properties of MCF-7 Luminal Breast Cancer Cells
by Ana Carolina Tirado-Garibay, Betzabe Ruiz-Barcenas, Julia Isabel Rescala-Ponce de León, Alejandra Ochoa-Zarzosa and Joel E. López-Meza
Int. J. Mol. Sci. 2024, 25(16), 8988; https://doi.org/10.3390/ijms25168988 - 18 Aug 2024
Viewed by 1106
Abstract
Luminal breast cancer has a high incidence worldwide and poses a severe health threat. Estrogen receptor alpha (ER-α) is activated by 17β-estradiol (E2), and its overexpression promotes cancerous characteristics. Luminal breast cancer is an epithelial type; however, the cytokine IL-6, secreted by cells [...] Read more.
Luminal breast cancer has a high incidence worldwide and poses a severe health threat. Estrogen receptor alpha (ER-α) is activated by 17β-estradiol (E2), and its overexpression promotes cancerous characteristics. Luminal breast cancer is an epithelial type; however, the cytokine IL-6, secreted by cells within the tumor microenvironment, stimulates the epithelial-to-mesenchymal transition (EMT) and promotes metastasis. Also, IL-6 decreases ER-α levels, favoring the tamoxifen (TMX) resistance development. However, genes under E2 regulation continue to be expressed even though this receptor is absent. GPR30 is an alternative E2 receptor present in both luminal and aggressive triple-negative breast cancer and is related to TMX resistance and cancer progression. The roles of GPR30 and IL-6 in metastasis have been individually established; however, their interplay remains unexplored. This study aims to elucidate the role of GPR30 in IL-6-induced metastatic properties of MCF-7 luminal breast cancer cells. Results showed that GPR30 contributes to the E2-induced MCF-7 proliferation because its inhibition with the antagonist G15 and the Pertussis toxin (PTX) reduced it. Besides, GPR30 upregulated vimentin and downregulated E-cadherin levels in MCF-7 and TMX-resistant (R-TMX) cells and is also involved in the IL-6-induced migration, invasion, and TMX resistance in MCF-7 cells. In addition, in MDA-MB-231 triple-negative cells, both basal and IL-6-induced metastatic properties were related to GPR30 activity. These results indicate that the GPR30 receptor regulates the EMT induced by IL-6 in breast cancer cells. Full article
(This article belongs to the Special Issue The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies)
►▼ Show Figures

Figure 1

12 pages, 1565 KiB  
Article
Expression of Growth Hormone-Releasing Hormone and Its Receptor Splice Variants in a Cohort of Hungarian Pediatric Patients with Hematological and Oncological Disorders: A Pilot Study
by Éva Juhász, Zsuzsanna Szabó, Andrew V. Schally, József Király, Petra Fodor, Gábor Kónya, Balázs Dezső, Erzsébet Szabó, Gábor Halmos and Csongor Kiss
Int. J. Mol. Sci. 2024, 25(16), 8831; https://doi.org/10.3390/ijms25168831 - 14 Aug 2024
Cited by 1 | Viewed by 823
Abstract
Hematological and oncological diseases are still among the leading causes of childhood mortality. Expression of growth hormone-releasing hormone (GHRH) and its receptors (GHRH-R) has been previously demonstrated in various human tumors, but very limited findings are available about the presence and potential function [...] Read more.
Hematological and oncological diseases are still among the leading causes of childhood mortality. Expression of growth hormone-releasing hormone (GHRH) and its receptors (GHRH-R) has been previously demonstrated in various human tumors, but very limited findings are available about the presence and potential function of GHRH-Rs in oncological and hematological disorders of children. In this study, we aimed to investigate the expression of mRNA for GHRH and splice variant 1 (SV) of GHRH-R in 15 pediatric hematological/oncological specimens by RT-PCR. The presence and binding characteristics of GHRH-R protein were also studied by Western blot and ligand competition assays. Of the fifteen specimens studied, eleven pediatric samples (73%) showed the expression of mRNA for GHRH. These eleven samples also expressed mRNA for GHRH receptor SV1. GHRH-R protein was found to be expressed in two benign tumor samples and five malignant tumors examined by Western blot. The presence of specific, high affinity binding sites on GHRH-R was demonstrated in all of the seven human pediatric solid tumor samples investigated. Our results show that the expression of GHRH and SV1 of GHRH-R in hemato-oncological diseases in children can pave the way for further investigation of GHRH-Rs as potential molecular targets for diagnosis and therapy. Full article
(This article belongs to the Special Issue The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies)
►▼ Show Figures

Figure 1

27 pages, 5048 KiB  
Article
Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer
by Reetobrata Basu, Prateek Kulkarni, Deborah Swegan, Silvana Duran-Ortiz, Arshad Ahmad, Lydia J. Caggiano, Emily Davis, Christopher Walsh, Edward Brenya, Adeel Koshal, Rich Brody, Uday Sandbhor, Sebastian J. C. M. M. Neggers and John J. Kopchick
Int. J. Mol. Sci. 2024, 25(13), 7438; https://doi.org/10.3390/ijms25137438 - 6 Jul 2024
Cited by 2 | Viewed by 1555
Abstract
Chemotherapy treatment against pancreatic ductal adenocarcinoma (PDAC) is thwarted by tumoral activation of multiple therapy resistance pathways. The growth hormone (GH)–GH receptor (GHR) pair is a covert driver of multimodal therapy resistance in cancer and is overexpressed in PDAC tumors, yet the therapeutic [...] Read more.
Chemotherapy treatment against pancreatic ductal adenocarcinoma (PDAC) is thwarted by tumoral activation of multiple therapy resistance pathways. The growth hormone (GH)–GH receptor (GHR) pair is a covert driver of multimodal therapy resistance in cancer and is overexpressed in PDAC tumors, yet the therapeutic potential of targeting the same has not been explored. Here, we report that GHR expression is a negative prognostic factor in patients with PDAC. Combinations of gemcitabine with different GHR antagonists (GHRAs) markedly improve therapeutic outcomes in nude mice xenografts. Employing cultured cells, mouse xenografts, and analyses of the human PDAC transcriptome, we identified that attenuation of the multidrug transporter and epithelial-to-mesenchymal transition programs in the tumors underlie the observed augmentation of chemotherapy efficacy by GHRAs. Moreover, in human PDAC patients, GHR expression strongly correlates with a gene signature of tumor promotion and immune evasion, which corroborate with that in syngeneic tumors in wild-type vs. GH transgenic mice. Overall, we found that GH action in PDAC promoted a therapy-refractory gene signature in vivo, which can be effectively attenuated by GHR antagonism. Our results collectively present a proof of concept toward considering GHR antagonists to improve chemotherapeutic outcomes in the highly chemoresistant PDAC. Full article
(This article belongs to the Special Issue The Role of Hormonal Receptors in Cancer: Molecular Mechanisms and Targeted Therapies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop