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7.4
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Cancers
Special Issues
Hormone Signaling in Cancer
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Hormone Signaling in Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 22568

Special Issue Editors

Dr. Rosaria Benedetti

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Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: cancer; epigenetics; hormone signaling; drug discovery
Special Issues, Collections and Topics in MDPI journals
Dr. Antonella di Costanzo

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Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: epigenetics; cancer; precision medicine; sumoylation; signal transduction
Dr. Federica Sarno

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: drug discovery; cancer; epigenetics; pharmaceutical chemistry; enzymatic assay
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hormone cell signaling functions in transcriptional activation and gene expression, regulating key physiological processes. However, abnormal hormone levels increase the risk of hormone-dependent malignancies, metabolic disorders, and immune dysfunctions. Cellular proliferation, migration, angiogenesis, and drug resistance mechanisms are modulated by para- and autocrine hormonal stimulation, highlighting the importance of altered endocrine stimulation in the onset and maintenance of cancer. Hormonal stimulation mainly acts by binding to receptors expressed by target cells. In many cases, these receptors are found on the target cell surface, but some receptors are intracellular proteins located in the cytosol or the nucleus. The activation of receptors by external signaling molecules sets off a complex chain of events within the cell that can result in altered protein structure and function and/or changes in gene expression. The elucidation of complex hormone signaling factors converging into the regulation of normal cell function should provide insights into how disruption of these processes may contribute to cancer. In this Special Issue, we focus on hormonal carcinogenesis and pathways leading to hormone alterations; on crosstalk between the extracellular matrix, environmental signals, and cancer; as well as on promising molecules that may potentially open up new therapeutic options for the treatment of hormone-related/dependent cancers. Drug discovery efforts to identify novel hormone-directed therapeutic agents or new routes overcoming innate and acquired resistance to hormone therapy should create breakthroughs in the treatment of breast and prostate cancers, which, at present, account for the two most frequent cancers worldwide.

Dr. Rosaria Benedetti
Dr. Antonella di Costanzo
Dr. Federica Sarno
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. 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

  • cancer and hormone-dependency
  • para- and autocrine hormonal stimulation
  • hormone therapy and resistance phenomena
  • hormone signaling pathways in cancer

Published Papers (6 papers)

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Research

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12 pages, 2381 KiB  
Article
Integrated Analysis of Key Differentially Expressed Genes Identifies DBN1 as a Predictive Marker of Response to Endocrine Therapy in Luminal Breast Cancer
by Lutfi H. Alfarsi, Rokaya El Ansari, Brendah K. Masisi, Ruth Parks, Omar J Mohammed, Ian O. Ellis, Emad A. Rakha and Andrew R. Green
Cancers 2020, 12(6), 1549; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061549 - 12 Jun 2020
Cited by 6 | Viewed by 2112
Abstract
Endocrine therapy is the mainstay of adjuvant treatment for patients with luminal breast cancer. Despite ongoing advances in endocrine therapy to date, a proportion of patients ultimately develop endocrine resistance, resulting in failure of therapy and poor prognosis. Therefore, as part of the [...] Read more.
Endocrine therapy is the mainstay of adjuvant treatment for patients with luminal breast cancer. Despite ongoing advances in endocrine therapy to date, a proportion of patients ultimately develop endocrine resistance, resulting in failure of therapy and poor prognosis. Therefore, as part of the growing concept of personalised medicine, the need for identification of predictive markers of endocrine therapy response at an early stage, is recognised. The METABRIC series was used to identify differentially expressed genes (DEGs) in term of response to adjuvant endocrine therapy. Drebrin 1 (DBN1) was identified as a key DEG associated with response to hormone treatment. Next, large, well-characterised cohorts of primary luminal breast cancer with long-term follow-up were assessed at the mRNA and protein levels for the value of DBN1 as a prognostic marker in luminal breast cancer, as well as its potential for predicting the benefit of endocrine therapy. DBN1 positivity was associated with aggressive clinicopathological variables and poor patient outcomes. Importantly, high DBN1 expression predicted relapse patients who were subject to adjuvant endocrine treatment. Our results further demonstrate that DBN1 is an independent prognostic marker in luminal breast cancer. Its association with the response to endocrine therapy and outcome provides evidence for DBN1 as a potential biomarker in luminal breast cancer, particularly for the benefit of endocrine treatment. Further functional investigations into the mechanisms underlying sensitivity to endocrine therapy is required. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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Review

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22 pages, 954 KiB  
Review
Neuro-Signals from Gut Microbiota: Perspectives for Brain Glioma
by Giuseppina D’Alessandro, Clotilde Lauro, Deborah Quaglio, Francesca Ghirga, Bruno Botta, Flavia Trettel and Cristina Limatola
Cancers 2021, 13(11), 2810; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13112810 - 04 Jun 2021
Cited by 15 | Viewed by 4751
Abstract
Glioblastoma (GBM) is the most aggressive form of glioma tumor in adult brain. Among the numerous factors responsible for GBM cell proliferation and invasion, neurotransmitters such as dopamine, serotonin and glutamate can play key roles. Studies performed in mice housed in germ-free (GF) [...] Read more.
Glioblastoma (GBM) is the most aggressive form of glioma tumor in adult brain. Among the numerous factors responsible for GBM cell proliferation and invasion, neurotransmitters such as dopamine, serotonin and glutamate can play key roles. Studies performed in mice housed in germ-free (GF) conditions demonstrated the relevance of the gut-brain axis in a number of physiological and pathological conditions. The gut–brain communication is made possible by vagal/nervous and blood/lymphatic routes and pave the way for reciprocal modulation of functions. The gut microbiota produces and consumes a wide range of molecules, including neurotransmitters (dopamine, norepinephrine, serotonin, gamma-aminobutyric acid [GABA], and glutamate) that reach their cellular targets through the bloodstream. Growing evidence in animals suggests that modulation of these neurotransmitters by the microbiota impacts host neurophysiology and behavior, and affects neural cell progenitors and glial cells, along with having effects on tumor cell growth. In this review we propose a new perspective connecting neurotransmitter modulation by gut microbiota to glioma progression. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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13 pages, 11815 KiB  
Review
Pigment Epithelium-Derived Factor and Sex Hormone-Responsive Cancers
by Naomi Brook, Emily Brook, Crispin R. Dass, Arlene Chan and Arun Dharmarajan
Cancers 2020, 12(11), 3483; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12113483 - 23 Nov 2020
Cited by 10 | Viewed by 2621
Abstract
Oestrogens and androgens play important roles in normal and cancerous tissue and have been shown to negatively regulate pigment epithelium-derived factor (PEDF) expression in sex hormone-responsive tumours. PEDF suppresses tumour growth and its downregulation by oestrogen is implicated in tumorigenesis, metastasis, and progression. [...] Read more.
Oestrogens and androgens play important roles in normal and cancerous tissue and have been shown to negatively regulate pigment epithelium-derived factor (PEDF) expression in sex hormone-responsive tumours. PEDF suppresses tumour growth and its downregulation by oestrogen is implicated in tumorigenesis, metastasis, and progression. PEDF expression is reduced in cancerous tissue of the prostate, breast, ovary, and endometrium compared to their normal tissue counterparts, with a link between PEDF downregulation and sex hormone signalling observed in pre-clinical studies. PEDF reduces growth and metastasis of tumour cells by promoting apoptosis, inhibiting angiogenesis, increasing adhesion, and reducing migration. PEDF may also prevent treatment resistance in some cancers by downregulating oestrogen receptor signalling. By interacting with components of the tumour microenvironment, PEDF counteracts the proliferative and immunosuppressive effects of oestrogens, to ultimately reduce tumorigenesis and metastasis. In this review, we focus on sex hormone regulation of PEDF’s anti-tumour action in sex hormone-responsive tumours. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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22 pages, 2126 KiB  
Review
Dopamine D1 Receptor in Cancer
by Paweł Sobczuk, Michał Łomiak and Agnieszka Cudnoch-Jędrzejewska
Cancers 2020, 12(11), 3232; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12113232 - 02 Nov 2020
Cited by 25 | Viewed by 5315
Abstract
Dopamine is a biologically active compound belonging to catecholamines. It plays its roles in the human body, acting both as a circulating hormone and neurotransmitter. It acts through G-protein-coupled receptors divided into two subgroups: D1-like receptors (D1R and D5R) and D2-like receptors (D2R, [...] Read more.
Dopamine is a biologically active compound belonging to catecholamines. It plays its roles in the human body, acting both as a circulating hormone and neurotransmitter. It acts through G-protein-coupled receptors divided into two subgroups: D1-like receptors (D1R and D5R) and D2-like receptors (D2R, D3R, D4R). Physiologically, dopamine receptors are involved in central nervous system functions: motivation or cognition, and peripheral actions such as blood pressure and immune response modulation. Increasing evidence indicates that the dopamine D1 receptor may play a significant role in developing different human neoplasms. This receptor’s value was presented in the context of regulating various signaling pathways important in tumor development, including neoplastic cell proliferation, apoptosis, autophagy, migration, invasiveness, or the enrichment of cancer stem cells population. Recent studies proved that its activation by selective or non-selective agonists is associated with significant tumor growth suppression, metastases prevention, and tumor microvasculature maturation. It may also exert a synergistic anti-cancer effect when combined with tyrosine kinase inhibitors or temozolomide. This review provides a comprehensive insight into the heterogeneity of dopamine D1 receptor molecular roles and signaling pathways in human neoplasm development and discusses possible perspectives of its therapeutic targeting as an adjunct anti-cancer strategy of treatment. We highlight the priorities for further directions in this research area. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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19 pages, 521 KiB  
Review
CDK4/6 Inhibitors in Hormone Receptor-Positive Metastatic Breast Cancer: Current Practice and Knowledge
by Debora de Melo Gagliato, Antonio C Buzaid, Jose Manuel Perez-Garcia, Antonio Llombart and Javier Cortes
Cancers 2020, 12(9), 2480; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12092480 - 01 Sep 2020
Cited by 14 | Viewed by 3486
Abstract
Treatment paradigms in advanced hormone receptor (HR)-positive breast cancer were substantially transformed with cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) approval. The addition of these drugs to endocrine treatment profoundly improved progression-free and overall survival. Additionally, other important endpoints, such as the response [...] Read more.
Treatment paradigms in advanced hormone receptor (HR)-positive breast cancer were substantially transformed with cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) approval. The addition of these drugs to endocrine treatment profoundly improved progression-free and overall survival. Additionally, other important endpoints, such as the response rate, time to chemotherapy, and a delay in quality of life deterioration, were positively impacted by CDK4/6 inhibitors’ addition to the treatment of advanced HR-positive breast cancer. This review article will summarize current knowledge on CDK4/6 inhibitors in clinical practice for advanced HR-positive metastatic breast cancer, as well as describe recent efforts to more precisely characterize mechanisms of sensitivity and resistance to these drugs, both on the molecular and clinical characterization level. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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33 pages, 2075 KiB  
Review
Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
by George Tzanakakis, Eirini-Maria Giatagana, Andrey Kuskov, Aikaterini Berdiaki, Aristidis Tsatsakis, Monica Neagu and Dragana Nikitovic
Cancers 2020, 12(9), 2401; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12092401 - 24 Aug 2020
Cited by 21 | Viewed by 3348
Abstract
Hormone-dependent cancers exhibit high morbidity and mortality. In spite of advances in therapy, the treatment of hormone-dependent cancers remains an unmet health need. The tumor microenvironment (TME) exhibits unique characteristics that differ among various tumor types. It is composed of cancerous, non-cancerous, stromal, [...] Read more.
Hormone-dependent cancers exhibit high morbidity and mortality. In spite of advances in therapy, the treatment of hormone-dependent cancers remains an unmet health need. The tumor microenvironment (TME) exhibits unique characteristics that differ among various tumor types. It is composed of cancerous, non-cancerous, stromal, and immune cells that are surrounded and supported by components of the extracellular matrix (ECM). Therefore, the interactions among cancer cells, stromal cells, and components of the ECM determine cancer progression and response to therapy. Proteoglycans (PGs), hybrid molecules consisting of a protein core to which sulfated glycosaminoglycan chains are bound, are significant components of the ECM that are implicated in all phases of tumorigenesis. These molecules, secreted by both the stroma and cancer cells, are crucial signaling mediators that modulate the vital cellular pathways implicated in gene expression, phenotypic versatility, and response to therapy in specific tumor types. A plethora of deregulated signaling pathways contributes to the growth, dissemination, and angiogenesis of hormone-dependent cancers. Specific inputs from the endocrine and immune systems are some of the characteristics of hormone-dependent cancer pathogenesis. Importantly, the mechanisms involved in various aspects of cancer progression are executed in the ECM niche of the TME, and the PG components crucially mediate these processes. Here, we comprehensively discuss the mechanisms through which PGs affect the multifaceted aspects of hormone-dependent cancer development and progression, including cancer metastasis, angiogenesis, immunobiology, autophagy, and response to therapy. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancer)
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