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Cancers
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Molecular Mechanisms in Prostate Cancer Development
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Molecular Mechanisms in Prostate Cancer Development

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (1 July 2024) | Viewed by 8094

Special Issue Editor

Dr. Yutaka Hashimoto

E-Mail Website
Guest Editor
Department of Urology, Urology Research Center, Veterans Affairs Medical Center and University of California San Francisco School of Medicine (UCSF), San Francisco, CA 94121, USA
Interests: prostate cancer; epigenomics; racial health disparity; noncoding RNA; biomarker; cancer etiology; metal toxicity; PI3K/Akt pathway

Special Issue Information

Dear Colleagues,

We are delighted to announce that new submissions are requested for the Special Issue entitled "Molecular Mechanisms in Prostate Cancer Development".

Prostate cancer (PCa) is common cancer, mostly diagnosed in men. More than 90% of cases without advanced PCa are not fatal, but the patient's quality of life could be impacted due to its high incidence rate. Recent developments in technologies have revealed many new mechanisms underlying PCa initiation and progression. However, we are still struggling to cure and control this disease. In the meantime, African American (AA) men are twice as likely to develop and die of PCa than their European American (EA) counterparts. This racial disparity has been attributed to differences in tumor growth rates and disease aggressiveness, and advanced disease leads to worse outcomes in AA men than EA men. Despite these facts, differences in genomic features between AA and EA PCa have also been highly understudied.

This Special Issue focuses on the molecular mechanisms of PCa initiation and progression, including drug resistance. Particularly, the molecular mechanism of racial health disparity and the relation of cancer immunology in PCa are very immature currently in the PCa research field. In addition, noncoding RNAs still play critical roles, and their application as biomarkers will be essential to predict disease and prognosis. Therefore, we should also keep a close eye on the "distance" between these epigenetic entities and each PCa molecular mechanism and pathway.

Any type of article, such as original research articles and reviews, is welcome if those are featured molecular mechanisms in prostate cancer development.

We look forward to receiving your contributions.

Dr. Yutaka Hashimoto
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 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

  • prostate cancer
  • epigenomics
  • racial health disparity
  • noncoding RNA
  • drug resistance
  • cancer etiology
  • metal toxicity
  • cancer immunology

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Published Papers (3 papers)

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Research

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18 pages, 9824 KiB  
Article
ID2 Promotes Lineage Transition of Prostate Cancer through FGFR and JAK-STAT Signaling
by Jinxiong Zhang, Zhihao Chen, Yongxin Mao, Yijun He, Xin Wu, Jianhong Wu and Lu Sheng
Cancers 2024, 16(2), 392; https://doi.org/10.3390/cancers16020392 - 17 Jan 2024
Viewed by 1497
Abstract
The use of androgen receptor pathway inhibitors (ARPIs) has led to an increase in the proportion of AR-null prostate cancer, including neuroendocrine prostate cancer (NEPC) and double-negative prostate cancer (DNPC), but the mechanism underlying this lineage transition has not been elucidated. We found [...] Read more.
The use of androgen receptor pathway inhibitors (ARPIs) has led to an increase in the proportion of AR-null prostate cancer, including neuroendocrine prostate cancer (NEPC) and double-negative prostate cancer (DNPC), but the mechanism underlying this lineage transition has not been elucidated. We found that ID2 expression was increased in AR-null prostate cancer. In vitro and in vivo studies confirmed that ID2 promotes PCa malignancy and can confer resistance to enzalutamide in PCa cells. We generated an ID2 UP50 signature, which is capable of determining resistance to enzalutamide and is valuable for predicting patient prognosis. Functional experiments showed that ID2 could activate stemness-associated JAK/STAT and FGFR signaling while inhibiting the AR signaling pathway. Our study indicates a potentially strong association between ID2 and the acquisition of a stem-like phenotype in adenocarcinoma cells, leading to resistance to androgen deprivation therapy (ADT) and next-generation ARPIs in prostate cancer. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Prostate Cancer Development)
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16 pages, 6526 KiB  
Article
Unveiling Disrupted Lipid Metabolism in Benign Prostate Hyperplasia, Prostate Cancer, and Metastatic Patients: Insights from a Colombian Nested Case–Control Study
by Daniel Pardo-Rodriguez, Mary Santamaría-Torres, Angela Salinas, Eliécer Jiménez-Charris, Mildrey Mosquera, Mónica P. Cala and Herney Andrés García-Perdomo
Cancers 2023, 15(22), 5465; https://doi.org/10.3390/cancers15225465 - 18 Nov 2023
Cited by 1 | Viewed by 1591
Abstract
Prostate cancer is a significant global health concern, and its prevalence is increasing worldwide. Despite extensive research efforts, the complexity of the disease remains challenging with respect to fully understanding it. Metabolomics has emerged as a powerful approach to understanding prostate cancer by [...] Read more.
Prostate cancer is a significant global health concern, and its prevalence is increasing worldwide. Despite extensive research efforts, the complexity of the disease remains challenging with respect to fully understanding it. Metabolomics has emerged as a powerful approach to understanding prostate cancer by assessing comprehensive metabolite profiles in biological samples. In this study, metabolic profiles of patients with benign prostatic hyperplasia (BPH), prostate cancer (PCa), and metastatic prostate cancer (Met) were characterized using an untargeted approach that included metabolomics and lipidomics via liquid chromatography and gas chromatography coupled with high-resolution mass spectrometry. Comparative analysis among these groups revealed distinct metabolic profiles, primarily associated with lipid biosynthetic pathways, such as biosynthesis of unsaturated fatty acids, fatty acid degradation and elongation, and sphingolipid and linoleic acid metabolism. PCa patients showed lower levels of amino acids, glycerolipids, glycerophospholipids, sphingolipids, and carnitines compared to BPH patients. Compared to Met patients, PCa patients had reduced metabolites in the glycerolipid, glycerophospholipid, and sphingolipid groups, along with increased amino acids and carbohydrates. These altered metabolic profiles provide insights into the underlying pathways of prostate cancer’s progression, potentially aiding the development of new diagnostic, and therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Prostate Cancer Development)
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Review

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34 pages, 574 KiB  
Review
Molecular Mechanisms of Prostate Cancer Development in the Precision Medicine Era: A Comprehensive Review
by Shigekatsu Maekawa, Ryo Takata and Wataru Obara
Cancers 2024, 16(3), 523; https://doi.org/10.3390/cancers16030523 - 25 Jan 2024
Cited by 3 | Viewed by 4416
Abstract
The progression of prostate cancer (PCa) relies on the activation of the androgen receptor (AR) by androgens. Despite efforts to block this pathway through androgen deprivation therapy, resistance can occur through several mechanisms, including the abnormal activation of AR, resulting in castration-resistant PCa [...] Read more.
The progression of prostate cancer (PCa) relies on the activation of the androgen receptor (AR) by androgens. Despite efforts to block this pathway through androgen deprivation therapy, resistance can occur through several mechanisms, including the abnormal activation of AR, resulting in castration-resistant PCa following the introduction of treatment. Mutations, amplifications, and splicing variants in AR-related genes have garnered attention in this regard. Furthermore, recent large-scale next-generation sequencing analysis has revealed the critical roles of AR and AR-related genes, as well as the DNA repair, PI3K, and cell cycle pathways, in the onset and progression of PCa. Moreover, research on epigenomics and microRNA has increasingly become popular; however, it has not translated into the development of effective therapeutic strategies. Additionally, treatments targeting homologous recombination repair mutations and the PI3K/Akt pathway have been developed and are increasingly accessible, and multiple clinical trials have investigated the efficacy of immune checkpoint inhibitors. In this comprehensive review, we outline the status of PCa research in genomics and briefly explore potential future developments in the field of epigenetic modifications and microRNAs. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Prostate Cancer Development)
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