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Molecular Biology of Prostate Cancer
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Molecular Biology of Prostate Cancer

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

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 9387

Special Issue Editor

Prof. Dr. Yukio Naya

E-Mail Website
Guest Editor
Department of Urology, Teikyo University Medical Center, Ichihara City, Japan
Interests: urinary bladder neoplasms; prostatic neoplasms; microrna; abiraterone cetate; castration-resistant prostatic neoplasms

Special Issue Information

Dear Colleagues,

Prostate cancer (PC) is the most common type of cancer among men and the second death rate of male cancer worldwide, with a new 1.4 million cases of incidence and 375,304 mortalities in 2020.

The etiology of prostate cancer remains largely unknown; in addition to aging and ethnicity, genetic and environmental factors are believed to contribute to the development of prostate cancer. Prostate cancer is characterized as molecularly heterogeneous, and its natural history is highly variable, which leads to different treatment modalities from active surveillance to aggressive treatment. Understanding these biological alterations behind is crucial in determining the course of the disease and providing a guide for therapy. Although most prostate cancers initially respond to androgen deprivation therapy (ADT), they gradually develop resistance and progress to castration-resistant prostate cancer (CRPC), which eventually becomes lethal. Understanding the mechanisms of CRPC will help us to develop novel treatment strategies and predict drug response toward precision medicine.

We invite researchers working on the identification of innovative strategies targeting PC to contribute to this Special Issue. Original research articles or reviews on ADT or CRPC related to the molecular and cellular mechanisms through which  Prostate cancer can be treated are welcome. Articles with insights on biological and therapeutic perspectives are especially welcome.

Prof. Dr. Yukio Naya
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

  • prostate cancer
  • ADT
  • CRPC
  • drug discovery
  • precision medicine

Published Papers (5 papers)

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Research

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15 pages, 1483 KiB  
Article
Transcripts of the Prostate Cancer-Associated Gene ANO7 Are Retained in the Nuclei of Prostatic Epithelial Cells
by Olli Metsälä, Gudrun Wahlström, Pekka Taimen, Pirkko-Liisa Kellokumpu-Lehtinen and Johanna Schleutker
Int. J. Mol. Sci. 2023, 24(2), 1052; https://doi.org/10.3390/ijms24021052 - 5 Jan 2023
Viewed by 1495
Abstract
Prostate cancer affects millions of men globally. The prostate cancer-associated gene ANO7 is downregulated in advanced prostate cancer, whereas benign tissue and low-grade cancer display varying expression levels. In this study, we assess the spatial correlation between ANO7 mRNA and protein using fluorescent [...] Read more.
Prostate cancer affects millions of men globally. The prostate cancer-associated gene ANO7 is downregulated in advanced prostate cancer, whereas benign tissue and low-grade cancer display varying expression levels. In this study, we assess the spatial correlation between ANO7 mRNA and protein using fluorescent in situ hybridization and immunohistochemistry for the detection of mRNA and protein in parallel sections of tissue microarrays prepared from radical prostatectomy samples. We show that ANO7 mRNA and protein expression correlate in prostate tissue. Furthermore, we show that ANO7 mRNA is enriched in the nuclei of the luminal cells at 89% in benign ducts and low-grade cancer, and at 78% in high-grade cancer. The nuclear enrichment of ANO7 mRNA was validated in prostate cancer cell lines 22Rv1 and MDA PCa 2b using droplet digital polymerase chain reaction (ddPCR) on RNA isolated from nuclear and cytoplasmic fractions of the cells. The nuclear enrichment of ANO7 mRNA was compared to the nuclearly-enriched lncRNA MALAT1, confirming the surprisingly high nuclear retention of ANO7 mRNA. ANO7 has been suggested to be used as a diagnostic marker and a target for immunotherapy, but a full comprehension of its role in prostate cancer progression is currently lacking. Our results contribute to a better understanding of the dynamics of ANO7 expression in prostatic tissue. Full article
(This article belongs to the Special Issue Molecular Biology of Prostate Cancer)
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18 pages, 2152 KiB  
Article
The Impact of Indoles Activating the Aryl Hydrocarbon Receptor on Androgen Receptor Activity in the 22Rv1 Prostate Cancer Cell Line
by Eliška Zgarbová and Radim Vrzal
Int. J. Mol. Sci. 2023, 24(1), 502; https://doi.org/10.3390/ijms24010502 - 28 Dec 2022
Cited by 1 | Viewed by 1654
Abstract
The activation of the aryl hydrocarbon receptor (AhR) by xenobiotic compounds was demonstrated to result in the degradation of the androgen receptor (AR). Since prostate cancer is often dependent on AR, it has become a significant therapeutic target. As a result of the [...] Read more.
The activation of the aryl hydrocarbon receptor (AhR) by xenobiotic compounds was demonstrated to result in the degradation of the androgen receptor (AR). Since prostate cancer is often dependent on AR, it has become a significant therapeutic target. As a result of the emerging concept of bacterial mimicry, we tested whether compounds with indole scaffolds capable of AhR activation have the potential to restrict AR activity in prostate cancer cells. Altogether, 22 indolic compounds were tested, and all of them activated AhR. However, only eight decreased DHT-induced AR luciferase activity. All indoles, which met the AhR-activating and AR-suppressing criteria, decreased the expression of DHT-inducible AR target genes, specifically KLK3 and FKBP5 mRNAs. The reduced AR binding to the KLK3 promoter was confirmed by a chromatin immunoprecipitation (ChIP) assay. In addition, some indoles significantly decreased AR protein and mRNA level. By using CRISPR/Cas9 AhR knockout technology, no relationship between AhR and AR, measured as target gene expression, was observed. In conclusion, some indoles that activate AhR possess AR-inhibiting activity, which seems to be related to the downregulation of AR expression rather than to AR degradation alone. Moreover, there does not seem to be a clear relationship that would connect AhR activation with AR activity suppression in 22Rv1 cells. Full article
(This article belongs to the Special Issue Molecular Biology of Prostate Cancer)
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20 pages, 5004 KiB  
Article
Macrophage-Colony-Stimulating Factor Receptor Enhances Prostate Cancer Cell Growth and Aggressiveness In Vitro and In Vivo and Increases Osteopontin Expression
by Alexandra Mougel, Eric Adriaenssens, Boris Guyot, Lu Tian, Stéphanie Gobert, Thierry Chassat, Philippe Persoons, David Hannebique, Hélène Bauderlique-Le Roy, Jérôme Vicogne, Xuefen Le Bourhis and Roland P. Bourette
Int. J. Mol. Sci. 2022, 23(24), 16028; https://doi.org/10.3390/ijms232416028 - 16 Dec 2022
Cited by 2 | Viewed by 1672
Abstract
Prostate cancer is a major public health concern and one of the most prevalent forms of cancer worldwide. The definition of altered signaling pathways implicated in this complex disease is thus essential. In this context, abnormal expression of the receptor of Macrophage Colony-Stimulating [...] Read more.
Prostate cancer is a major public health concern and one of the most prevalent forms of cancer worldwide. The definition of altered signaling pathways implicated in this complex disease is thus essential. In this context, abnormal expression of the receptor of Macrophage Colony-Stimulating Factor-1 (M-CSF or CSF-1) has been described in prostate cancer cells. Yet, outcomes of this expression remain unknown. Using mouse and human prostate cancer cell lines, this study has investigated the functionality of the wild-type CSF-1 receptor in prostate tumor cells and identified molecular mechanisms underlying its ligand-induced activation. Here, we showed that upon CSF-1 binding, the receptor autophosphorylates and activates multiple signaling pathways in prostate tumor cells. Biological experiments demonstrated that the CSF-1R/CSF-1 axis conferred significant advantages in cell growth and cell invasion in vitro. Mouse xenograft experiments showed that CSF-1R expression promoted the aggressiveness of prostate tumor cells. In particular, we demonstrated that the ligand-activated CSF-1R increased the expression of spp1 transcript encoding for osteopontin, a key player in cancer development and metastasis. Therefore, this study highlights that the CSF-1 receptor is fully functional in a prostate cancer cell and may be a potential therapeutic target for the treatment of prostate cancer. Full article
(This article belongs to the Special Issue Molecular Biology of Prostate Cancer)
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Review

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14 pages, 3636 KiB  
Review
Cancer Stem Cells and Prostate Cancer: A Narrative Review
by Yazan Al Salhi, Manfredi Bruno Sequi, Fabio Maria Valenzi, Andrea Fuschi, Alessia Martoccia, Paolo Pietro Suraci, Antonio Carbone, Giorgia Tema, Riccardo Lombardo, Antonio Cicione, Antonio Luigi Pastore and Cosimo De Nunzio
Int. J. Mol. Sci. 2023, 24(9), 7746; https://doi.org/10.3390/ijms24097746 - 24 Apr 2023
Viewed by 1645
Abstract
Cancer stem cells (CSCs) are a small and elusive subpopulation of self-renewing cancer cells with the remarkable ability to initiate, propagate, and spread malignant disease. In the past years, several authors have focused on the possible role of CSCs in PCa development and [...] Read more.
Cancer stem cells (CSCs) are a small and elusive subpopulation of self-renewing cancer cells with the remarkable ability to initiate, propagate, and spread malignant disease. In the past years, several authors have focused on the possible role of CSCs in PCa development and progression. PCa CSCs typically originate from a luminal prostate cell. Three main pathways are involved in the CSC development, including the Wnt, Sonic Hedgehog, and Notch signaling pathways. Studies have observed an important role for epithelial mesenchymal transition in this process as well as for some specific miRNA. These studies led to the development of studies targeting these specific pathways to improve the management of PCa development and progression. CSCs in prostate cancer represent an actual and promising field of research. Full article
(This article belongs to the Special Issue Molecular Biology of Prostate Cancer)
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13 pages, 1485 KiB  
Review
Dependence on MUC1-C in Progression of Neuroendocrine Prostate Cancer
by Donald Kufe
Int. J. Mol. Sci. 2023, 24(4), 3719; https://doi.org/10.3390/ijms24043719 - 13 Feb 2023
Cited by 6 | Viewed by 2339
Abstract
Castration resistant prostate cancer (CRPC) is responsive to androgen receptor (AR) axis targeted agents; however, patients invariably relapse with resistant disease that often progresses to neuroendocrine prostate cancer (NEPC). Treatment-related NEPC (t-NEPC) is highly aggressive with limited therapeutic options and poor survival outcomes. [...] Read more.
Castration resistant prostate cancer (CRPC) is responsive to androgen receptor (AR) axis targeted agents; however, patients invariably relapse with resistant disease that often progresses to neuroendocrine prostate cancer (NEPC). Treatment-related NEPC (t-NEPC) is highly aggressive with limited therapeutic options and poor survival outcomes. The molecular basis for NEPC progression remains incompletely understood. The MUC1 gene evolved in mammals to protect barrier tissues from loss of homeostasis. MUC1 encodes the transmembrane MUC1-C subunit, which is activated by inflammation and contributes to wound repair. However, chronic activation of MUC1-C contributes to lineage plasticity and carcinogenesis. Studies in human NEPC cell models have demonstrated that MUC1-C suppresses the AR axis and induces the Yamanaka OSKM pluripotency factors. MUC1-C interacts directly with MYC and activates the expression of the BRN2 neural transcription factor (TF) and other effectors, such as ASCL1, of the NE phenotype. MUC1-C also induces the NOTCH1 stemness TF in promoting the NEPC cancer stem cell (CSC) state. These MUC1-C-driven pathways are coupled with activation of the SWI/SNF embryonic stem BAF (esBAF) and polybromo-BAF (PBAF) chromatin remodeling complexes and global changes in chromatin architecture. The effects of MUC1-C on chromatin accessibility integrate the CSC state with the control of redox balance and induction of self-renewal capacity. Importantly, targeting MUC1-C inhibits NEPC self-renewal, tumorigenicity and therapeutic resistance. This dependence on MUC1-C extends to other NE carcinomas, such as SCLC and MCC, and identify MUC1-C as a target for the treatment of these aggressive malignancies with the anti-MUC1 agents now under clinical and preclinical development. Full article
(This article belongs to the Special Issue Molecular Biology of Prostate Cancer)
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