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Hormone Signaling in Cancers and Cancer-Promoting Pathologies
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Hormone Signaling in Cancers and Cancer-Promoting Pathologies

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 April 2025 | Viewed by 10296

Special Issue Editor

Dr. Olga Sukocheva

E-Mail Website1 Website2 Website3
Guest Editor
Lecturer in Health Sciences, College of Nursing and Health Sciences, Flinders University of South Australia, Adelaide 5001, Australia
Interests: breast cancer; oesophageal adenocarcinoma; oestrogen receptors; sphingolipids; breast cancer stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The endocrine system and hormones control key physiological processes associated with carcinogenesis. Transported via the bloodstream, hormones have been shown to integrate and coordinate virtually all physiological processes. Hormone signaling is responsible for transcriptional activation and regulation of gene expression, observed during changes in cellular growth, embryonic development, differentiation, and metabolism. Hormone receptors mediate pro-oncogenic functions in several cancer histotypes and trigger molecular programs involved in the regulation of a wide array of biological effects which promote tumor cell proliferation, migration, invasion, survival, and development of resistance to anticancer therapy.

Radical contributions of steroid hormones (such as estrogen, progesterone, and androgen) to the development of breast and prostate malignancies have been reported in numerous research studies, although mechanisms of steroid hormone signaling and therapeutic approaches to control this signaling remain to be deciphered. Cancer-linked pathological changes in energy metabolism, including obesity, have also been shown to be under hormonal control. It is crucial to define the mechanisms through which hormones regulate energy homeostasis during carcinogenesis in the targeted tissues. The essential role of hormones has been observed during the resolution and progression of inflammation, another contributor of cancer progression. The interaction of pro-inflammatory cytokines and hormones signaling pathways is one of the most complex and puzzling networks in carcinogenesis. Aside from the involvement of hormone receptors (and their target genes) and downstream effectors, hormone actions are coordinated by a complex apparatus of transcriptional (mRNA and noncoding RNA) and epigenetic machinery, which can modulate protein expression and function and reprogram cell metabolism.

This Special Issue aims to address open questions in the regulation and function of hormone receptors in cancers and cancer-related pathologies, and pathways leading to alterations in hormone signaling mechanisms. We propose to submit manuscripts that address the role of hormones in the regulation of energy metabolism, inflammation, and other cancer-linked mechanism of cell transformation. The submission of studies that investigate or discuss epigenetic regulation of hormone signaling in cancers and cancer-preceding pathologies is also welcome.

Dr. Olga Sukocheva
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

  • estrogen
  • androgen
  • thyroxine
  • thyroid hormones
  • adrenalin
  • adrenocorticoids
  • progesterone
  • medroxyprogesterone
  • mifepristone
  • corticosteroids
  • glucocorticoids
  • mineralocorticoids
  • testosterone
  • cortisol
  • prednisolone
  • hormones
  • hormone receptors
  • endocrine-related cancers
  • hormone therapy
  • hormone therapy resistance
  • drug resistance
  • epigenetics
  • microRNA

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Published Papers (4 papers)

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Research

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24 pages, 14241 KiB  
Article
Pigmented Microbial Extract (PMB) from Exiguobacterium Species MB2 Strain (PMB1) and Bacillus subtilis Strain MB1 (PMB2) Inhibited Breast Cancer Cells Growth In Vivo and In Vitro
by Deepa R. Bandi, Ch M. Kumari Chitturi, Jamuna Bai Aswathanarayan, Prashant Kumar M. Veeresh, Venugopal R. Bovilla, Olga A. Sukocheva, Potireddy Suvarnalatha Devi, Suma M. Natraj and SubbaRao V. Madhunapantula
Int. J. Mol. Sci. 2023, 24(24), 17412; https://doi.org/10.3390/ijms242417412 - 12 Dec 2023
Viewed by 1491
Abstract
Breast cancer (BC) continues to be one of the major causes of cancer deaths in women. Progress has been made in targeting hormone and growth factor receptor-positive BCs with clinical efficacy and success. However, little progress has been made to develop a clinically [...] Read more.
Breast cancer (BC) continues to be one of the major causes of cancer deaths in women. Progress has been made in targeting hormone and growth factor receptor-positive BCs with clinical efficacy and success. However, little progress has been made to develop a clinically viable treatment for the triple-negative BC cases (TNBCs). The current study aims to identify potent agents that can target TNBCs. Extracts from microbial sources have been reported to contain pharmacological agents that can selectively inhibit cancer cell growth. We have screened and identified pigmented microbial extracts (PMBs) that can inhibit BC cell proliferation by targeting legumain (LGMN). LGMN is an oncogenic protein expressed not only in malignant cells but also in tumor microenvironment cells, including tumor-associated macrophages. An LGMN inhibition assay was performed, and microbial extracts were evaluated for in vitro anticancer activity in BC cell lines, angiogenesis assay with chick chorioallantoic membrane (CAM), and tumor xenograft models in Swiss albino mice. We have identified that PMB from the Exiguobacterium (PMB1), inhibits BC growth more potently than PMB2, from the Bacillus subtilis strain. The analysis of PMB1 by GC-MS showed the presence of a variety of fatty acids and fatty-acid derivatives, small molecule phenolics, and aldehydes. PMB1 inhibited the activity of oncogenic legumain in BC cells and induced cell cycle arrest and apoptosis. PMB1 reduced the angiogenesis and inhibited BC cell migration. In mice, intraperitoneal administration of PMB1 retarded the growth of xenografted Ehrlich ascites mammary tumors and mitigated the proliferation of tumor cells in the peritoneal cavity in vivo. In summary, our findings demonstrate the high antitumor potential of PMB1. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancers and Cancer-Promoting Pathologies)
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16 pages, 14813 KiB  
Article
Intratumoral Restoration of miR-137 Plus Cholesterol Favors Homeostasis of the miR-137/Coactivator p160/AR Axis and Negatively Modulates Tumor Progression in Advanced Prostate Cancer
by Ruan Pimenta, Carolina Mie Mioshi, Guilherme L. Gonçalves, Patrícia Candido, Juliana A. Camargo, Vanessa R. Guimarães, Caroline Chiovatto, Vitória Ghazarian, Poliana Romão, Karina Serafim da Silva, Gabriel A. dos Santos, Iran A. Silva, Miguel Srougi, William C. Nahas, Kátia R. Leite, Nayara I. Viana and Sabrina T. Reis
Int. J. Mol. Sci. 2023, 24(11), 9633; https://doi.org/10.3390/ijms24119633 - 1 Jun 2023
Cited by 4 | Viewed by 1873
Abstract
MicroRNAs (miRNAs) have gained a prominent role as biomarkers in prostate cancer (PCa). Our study aimed to evaluate the potential suppressive effect of miR-137 in a model of advanced PCa with and without diet-induced hypercholesterolemia. In vitro, PC-3 cells were treated with 50 [...] Read more.
MicroRNAs (miRNAs) have gained a prominent role as biomarkers in prostate cancer (PCa). Our study aimed to evaluate the potential suppressive effect of miR-137 in a model of advanced PCa with and without diet-induced hypercholesterolemia. In vitro, PC-3 cells were treated with 50 pmol of mimic miR-137 for 24 h, and gene and protein expression levels of SRC-1, SRC-2, SRC-3, and AR were evaluated by qPCR and immunofluorescence. We also assessed migration rate, invasion, colony-forming ability, and flow cytometry assays (apoptosis and cell cycle) after 24 h of miRNA treatment. For in vivo experiments, 16 male NOD/SCID mice were used to evaluate the effect of restoring miR-137 expression together with cholesterol. The animals were fed a standard (SD) or hypercholesterolemic (HCOL) diet for 21 days. After this, we xenografted PC-3 LUC-MC6 cells into their subcutaneous tissue. Tumor volume and bioluminescence intensity were measured weekly. After the tumors reached 50 mm3, we started intratumor treatments with a miR-137 mimic, at a dose of 6 μg weekly for four weeks. Ultimately, the animals were killed, and the xenografts were resected and analyzed for gene and protein expression. The animals’ serum was collected to evaluate the lipid profile. The in vitro results showed that miR-137 could inhibit the transcription and translation of the p160 family, SRC-1, SRC-2, and SRC-3, and indirectly reduce the expression of AR. After these analyses, it was determined that increased miR-137 inhibits cell migration and invasion and impacts reduced proliferation and increased apoptosis rates. The in vivo results demonstrated that tumor growth was arrested after the intratumoral restoration of miR-137, and proliferation levels were reduced in the SD and HCOL groups. Interestingly, the tumor growth retention response was more significant in the HCOL group. We conclude that miR-137 is a potential therapeutic miRNA that, in association with androgen precursors, can restore and reinstate the AR-mediated axis of transcription and transactivation of androgenic pathway homeostasis. Further studies involving the miR-137/coregulator/AR/cholesterol axis should be conducted to evaluate this miR in a clinical context. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancers and Cancer-Promoting Pathologies)
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12 pages, 3327 KiB  
Article
Functional and Phenotypic Characterisations of Common Syngeneic Tumour Cell Lines as Estrogen Receptor-Positive Breast Cancer Models
by Maria Lambouras, Charlotte Roelofs, Melrine Pereira, Emily Gruber, Jessica L. Vieusseux, Patrick Lanteri, Cameron N. Johnstone, Fenella Muntz, Sandra O’Toole, Lisa M. Ooms, Christina A. Mitchell, Robin L. Anderson and Kara L. Britt
Int. J. Mol. Sci. 2023, 24(6), 5666; https://doi.org/10.3390/ijms24065666 - 16 Mar 2023
Cited by 2 | Viewed by 2944
Abstract
Estrogen receptor-positive breast cancers (ER+ BCas) are the most common form of BCa and are increasing in incidence, largely due to changes in reproductive practices in recent decades. Tamoxifen is prescribed as a component of standard-of-care endocrine therapy for the treatment and [...] Read more.
Estrogen receptor-positive breast cancers (ER+ BCas) are the most common form of BCa and are increasing in incidence, largely due to changes in reproductive practices in recent decades. Tamoxifen is prescribed as a component of standard-of-care endocrine therapy for the treatment and prevention of ER+ BCa. However, it is poorly tolerated, leading to low uptake of the drug in the preventative setting. Alternative therapies and preventatives for ER+ BCa are needed but development is hampered due to a paucity of syngeneic ER+ preclinical mouse models that allow pre-clinical experimentation in immunocompetent mice. Two ER-positive models, J110 and SSM3, have been reported in addition to other tumour models occasionally shown to express ER (for example 4T1.2, 67NR, EO771, D2.0R and D2A1). Here, we have assessed ER expression and protein levels in seven mouse mammary tumour cell lines and their corresponding tumours, in addition to their cellular composition, tamoxifen sensitivity and molecular phenotype. By immunohistochemical assessment, SSM3 and, to a lesser extent, 67NR cells are ER+. Using flow cytometry and transcript expression we show that SSM3 cells are luminal in nature, whilst D2.0R and J110 cells are stromal/basal. The remainder are also stromal/basal in nature; displaying a stromal or basal Epcam/CD49f FACS phenotype and stromal and basal gene expression signatures are overrepresented in their transcript profile. Consistent with a luminal identity for SSM3 cells, they also show sensitivity to tamoxifen in vitro and in vivo. In conclusion, the data indicate that the SSM3 syngeneic cell line is the only definitively ER+ mouse mammary tumour cell line widely available for pre-clinical research. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancers and Cancer-Promoting Pathologies)
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Review

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21 pages, 1382 KiB  
Review
Meeting at the Crossroad between Obesity and Hepatic Carcinogenesis: Unique Pathophysiological Pathways Raise Expectations for Innovative Therapeutic Approaches
by Konstantinos Arvanitakis, Stavros P. Papadakos, Vasileios Lekakis, Theocharis Koufakis, Ioannis G. Lempesis, Eleni Papantoniou, Georgios Kalopitas, Vasiliki E. Georgakopoulou, Ioanna E. Stergiou, Stamatios Theocharis and Georgios Germanidis
Int. J. Mol. Sci. 2023, 24(19), 14704; https://doi.org/10.3390/ijms241914704 - 28 Sep 2023
Cited by 7 | Viewed by 2952
Abstract
The escalating global prevalence of obesity and its intricate association with the development of hepatocellular carcinoma (HCC) pose a substantial challenge to public health. Obesity, acknowledged as a pervasive epidemic, is linked to an array of chronic diseases, including HCC, catalyzing the need [...] Read more.
The escalating global prevalence of obesity and its intricate association with the development of hepatocellular carcinoma (HCC) pose a substantial challenge to public health. Obesity, acknowledged as a pervasive epidemic, is linked to an array of chronic diseases, including HCC, catalyzing the need for a comprehensive understanding of its molecular underpinnings. Notably, HCC has emerged as a leading malignancy with rising incidence and mortality. The transition from viral etiologies to the prominence of metabolic dysfunction-associated fatty liver disease (MAFLD)-related HCC underscores the urgent need to explore the intricate molecular pathways linking obesity and hepatic carcinogenesis. This review delves into the interwoven landscape of molecular carcinogenesis in the context of obesity-driven HCC while also navigating using the current therapeutic strategies and future prospects for combating obesity-related HCC. We underscore the pivotal role of obesity as a risk factor and propose an integrated approach encompassing lifestyle interventions, pharmacotherapy, and the exploration of emerging targeted therapies. As the obesity-HCC nexus continues to challenge healthcare systems globally, a comprehensive understanding of the intricate molecular mechanisms and innovative therapeutic strategies is imperative to alleviate the rising burden of this dual menace. Full article
(This article belongs to the Special Issue Hormone Signaling in Cancers and Cancer-Promoting Pathologies)
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