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Hormone Signaling in Human Health and Diseases 2.0

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

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1259

Special Issue Editor


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Guest Editor
Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Università del Salento, 73100 Lecce, Italy
Interests: signal transduction; hormones; apoptosis; autophagy; metabolism
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of the 2022 Special Issue “Hormone Signaling in Human Health and Diseases”.

Cell signaling is part of any communication process that regulates the basic activities of cells and coordinates all cellular actions. The ability of cells to perceive and respond correctly to their microenvironment underlies the development, repair of tissues, immunity and homeostasis of normal tissues. Errors in signaling interactions and cellular information processing are responsible for three large classes of non-infectious diseases: cancers, neurodegenerative disorders and metabolic syndromes (such as type 2 diabetes and atherosclerosis). These diseases are remarkably complex and difficult to treat, primarily because when the cellular signaling pathways responsible for homeostasis and the health of the body become dysregulated, they generate similarly stable disease states.

Health- and disease-related conditions are dynamic and positively and negatively regulated by different feedback loops acting between pathways. Hormones are common signaling agents. Understanding cell signaling, especially relating hormone signaling, and describing regulatory networks in healthy and diseased states will show which molecular components may be the prime targets for drug interventions to manage these diseases more effectively. This is accomplished by studying models that explain in mechanistic, molecular detail the way in which a detailed part of the hormone signaling pathway functions properly in health and abnormally in disease.

Dr. Antonella Muscella
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
  • cell receptor
  • endocrine signaling
  • cancer
  • insulin
  • oestrogen
  • testosterone
  • angiotensin
  • gonadotropin
  • thyroid hormone

Published Papers (1 paper)

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Research

16 pages, 3470 KiB  
Article
Androgens Modulate Bcl-2 Agonist of Cell Death (BAD) Expression and Function in Breast Cancer Cells
by Catia Morelli, Chiara Chiodo, Marta Claudia Nocito, Alessandro Cormace, Stefania Catalano, Diego Sisci, Rosa Sirianni, Ivan Casaburi, Sebastiano Andò and Marilena Lanzino
Int. J. Mol. Sci. 2023, 24(17), 13464; https://doi.org/10.3390/ijms241713464 - 30 Aug 2023
Cited by 2 | Viewed by 906
Abstract
Androgen receptor (AR) expression in estrogen receptor-positive (ER+) breast cancer (BC) correlates with lower tumor grade and a better clinical outcome. Additionally, in normal mammary epithelium or ER+ BC preclinical models, androgens counteract basal/ER-dependent proliferation. Here, we report an additional mechanism, underlining the [...] Read more.
Androgen receptor (AR) expression in estrogen receptor-positive (ER+) breast cancer (BC) correlates with lower tumor grade and a better clinical outcome. Additionally, in normal mammary epithelium or ER+ BC preclinical models, androgens counteract basal/ER-dependent proliferation. Here, we report an additional mechanism, underlining the protective role exerted by AR. Specifically, the activation of intracellular AR upregulates the Bcl-2-family protein BAD, and TCGA database analyses show that in ER+ BC, BAD expression is associated with better disease-free survival. Ligand-activated AR influences its own and BAD cellular compartmentalization by enhancing levels in the nucleus, as well as in mitochondrial fractions. In both compartments, BAD exerts unconventional functions. In the nucleus, BAD and AR physically interact and, upon androgen stimulation, are recruited at the AP-1 and ARE sites within the cyclin D1 promoter region, contributing to explaining the anti-proliferative effect of androgens in BC cells. Androgens cause an enrichment in BAD and AR content in the mitochondria, correlated with a decrease in mitochondrial function. Thus, we have defined a novel mechanism by which androgens modulate BAD expression, its mitochondria localization, and nuclear content to force its ability to act as a cell cycle inhibitor, strengthening the protective role of androgen signaling in estrogen-responsive BCs. Full article
(This article belongs to the Special Issue Hormone Signaling in Human Health and Diseases 2.0)
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