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Prostate Cancer: Pathology, Pathobiology and Therapy
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Prostate Cancer: Pathology, Pathobiology and Therapy

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: closed (15 May 2023) | Viewed by 16554

Special Issue Editors

Prof. Dr. Ajay Pratap Singh

E-Mail Website
Guest Editor
1. Department of Pathology, College of Medicine, University of South Alabama, Mobile, AL 36604, USA
2. Cancer Biology Program, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA
Interests: pancreatic cancer; prostate cancer; breast cancer; carcinogenesis; tumor microenvironment; metastasis; therapy resistance; gene regulation
Special Issues, Collections and Topics in MDPI journals
Dr. Debanjan Chakroborty

E-Mail Website
Guest Editor
Department of Pathology, University of South Alabama, Mobile, AL 36617, USA
Interests: tumor biology; tumor microenvironment; tumor metastasis; angiogenesis; targeted therapy; therapeutic resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prostate cancer is the most common malignancy (after skin cancer) and the second leading cause of cancer-related death among US men. The incidence of prostate cancer has also been increasing steadily worldwide. Due to disease heterogeneity, patients with prostate cancer show a range of prognoses and different treatment outcomes. Disparate incidence and clinical outcomes in different racial and ethnic groups are also common even when accounted for socioeconomic variables further adding to the complexity of the disease biology. Moreover, there is a lack of specific biomarkers leading to overdiagnosis of prostate cancer, which in turn results in unnecessary treatment, economic burden and psychological stress to the patients and their families. Clearly, an improved understanding of the prostate cancer pathology and pathobiology is critical to develop novel approaches for prostate cancer diagnosis, prognosis and therapy.

This Special Issue seeks research and review manuscripts focusing on the molecular and cellular basis of prostate cancer, biomarkers and emerging advances in disease stratification, mechanisms underlying therapeutic failure, aggressive behavior, and evaluation of novel therapeutic interventions.

Prof. Dr. Ajay Pratap Singh
Dr. Debanjan Chakroborty
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. 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/Prostatic adenocarcinoma
  • Biomarkers
  • Molecular subtyping
  • Metastasis
  • Angiogenesis
  • Tumor Microenvironment
  • Host-tumor interaction
  • Therapy resistance
  • Chemotherapy
  • Hormone Therapy
  • Targeted Therapy
  • Radiotherapy
  • Combination therapy

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

4 pages, 182 KiB  
Editorial
Prostate Cancer: Insights into Disease Progression and Therapeutic Challenges
by Debanjan Chakroborty and Ajay Pratap Singh
Int. J. Mol. Sci. 2024, 25(5), 2451; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25052451 - 20 Feb 2024
Viewed by 533
Abstract
Prostate cancer (PCa) is the second most common cancer and the fifth highest cause of cancer-related death among men in the world [...] Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)

Research

Jump to: Editorial, Review

18 pages, 5300 KiB  
Article
Androgen Receptor Upregulates Mucosa-Associated Lymphoid Tissue 1 to Induce NF-κB Activity via Androgen-Dependent and -Independent Pathways in Prostate Carcinoma Cells
by Kang-Shuo Chang, Syue-Ting Chen, Hsin-Ching Sung, Shu-Yuan Hsu, Wei-Yin Lin, Chen-Pang Hou, Yu-Hsiang Lin, Tsui-Hsia Feng, Ke-Hung Tsui and Horng-Heng Juang
Int. J. Mol. Sci. 2023, 24(7), 6245; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24076245 - 26 Mar 2023
Viewed by 1351
Abstract
The androgen-dependent or -independent pathways are regarded as primary therapeutic targets for the neoplasm of the prostate. Mucosa-associated lymphoid tissue 1 (MALT1) acting as a paracaspase in the regulation of nuclear factor κB (NF-κB) signal transduction plays a central role in inflammation and [...] Read more.
The androgen-dependent or -independent pathways are regarded as primary therapeutic targets for the neoplasm of the prostate. Mucosa-associated lymphoid tissue 1 (MALT1) acting as a paracaspase in the regulation of nuclear factor κB (NF-κB) signal transduction plays a central role in inflammation and oncogenesis in cancers. This study confirmed the potential linkages between androgen and NF-κB activation by inducing MALT1 in the androgen receptor-full length (ARFL)-positive LNCaP and 22Rv1 prostate cancer cells. Although androgen did not stimulate MALT1 expression in AR-null or ectopic ARFL-overexpressed PC-3 cells, the ectopic overexpression of the AR splicing variant 7 (ARv7) upregulated MALT1 to activate NF-κB activities in 22Rv1 and PC-3 cells. Since the nuclear translocation of p50 and p65 was facilitated by ARv7 to motivate NF-κB activity, the expressions of MALT1, prostate-specific antigen (PSA), and N-myc downstream regulated 1 (NDRG1) were therefore induced in ectopic ARv7-overexpressed prostate cancer cells. Ectopic ARv7 overexpression not only enhanced 22Rv1 or PC-3 cell growth and invasion in vitro but also the tumor growth of PC-3 cells in vivo. These results indicate that an androgen receptor induces MALT1 expression androgen-dependently and -independently in ARFL- or ARv7-overexpressed prostate cancer cells, suggesting a novel ARv7/MALT1/NF-κB-signaling pathway may exist in the cells of prostate cancer. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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Graphical abstract

17 pages, 2641 KiB  
Article
Early Cell Cultures from Prostate Cancer Tissue Express Tissue Specific Epithelial and Cancer Markers
by Vladimir M. Ryabov, Mikhail M. Baryshev, Mikhail A. Voskresenskiy and Boris V. Popov
Int. J. Mol. Sci. 2023, 24(3), 2830; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032830 - 01 Feb 2023
Viewed by 1790
Abstract
Prostate cancer (PCa) is a widespread oncological disease that proceeds in the indolent form in most patients. However, in some cases, the indolent form can transform into aggressive metastatic incurable cancer. The most important task of PCa diagnostics is to search for early [...] Read more.
Prostate cancer (PCa) is a widespread oncological disease that proceeds in the indolent form in most patients. However, in some cases, the indolent form can transform into aggressive metastatic incurable cancer. The most important task of PCa diagnostics is to search for early markers that can be used for predicting the transition of indolent cancer into its aggressive form. Currently, there are two effective preclinical models to study PCa pathogenesis: patients derived xenografts (PDXs) and patients derived organoids (PDOs). Both models have limitations that restrict their use in research. In this work, we investigated the ability of the primary 2D prostate cell cultures (PCCs) from PCa patients to express epithelial and cancer markers. Early PCCs were formed by epithelial cells that were progressively replaced with the fibroblast-like cells. Early PCCs contained tissue-specific stem cells that could grow in a 3D culture and form PDOs similar to those produced from the prostate tissue. Early PCCs and PDOs derived from the tissues of PCa patients expressed prostate basal and luminal epithelial markers, as well as cancer markers AMACR, TMPRSS2-ERG, and EZH2, the latter being a promising candidate to mark the transition from the indolent to aggressive PCa. We also identified various TMPRSS2-ERG fusion transcripts in PCCs and PDOs, including new chimeric variants resulting from the intra- and interchromosomal translocations. The results suggest that early PCCs derived from cancerous and normal prostate tissues sustain the phenotype of prostate cells and can be used as a preclinical model to study the pathogenesis of PCa. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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15 pages, 3508 KiB  
Article
Enhanced Antitumor Efficacy of Radium-223 and Enzalutamide in the Intratibial LNCaP Prostate Cancer Model
by Mari I. Suominen, Matias Knuuttila, Christoph A. Schatz, Andreas Schlicker, Jukka Vääräniemi, Birgitta Sjöholm, Esa Alhoniemi, Bernard Haendler, Dominik Mumberg, Sanna-Maria Käkönen and Arne Scholz
Int. J. Mol. Sci. 2023, 24(3), 2189; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032189 - 22 Jan 2023
Cited by 2 | Viewed by 2563
Abstract
Radium-223 dichloride and enzalutamide are indicated for metastatic castration-resistant prostate cancer and their combination is currently being investigated in a large phase 3 clinical trial. Here, we evaluated the antitumor efficacy of radium-223, enzalutamide, and their combination in the intratibial LNCaP model mimicking [...] Read more.
Radium-223 dichloride and enzalutamide are indicated for metastatic castration-resistant prostate cancer and their combination is currently being investigated in a large phase 3 clinical trial. Here, we evaluated the antitumor efficacy of radium-223, enzalutamide, and their combination in the intratibial LNCaP model mimicking prostate cancer metastasized to bone. In vitro experiments revealed that the combination of radium-223 and enzalutamide inhibited LNCaP cell proliferation and showed synergistic efficacy. The combination of radium-223 and enzalutamide also demonstrated enhanced in vivo antitumor efficacy, as determined by measuring serum PSA levels in the intratibial LNCaP model. A decreasing trend in the total area of tumor-induced abnormal bone was associated with the combination treatment. The serum levels of the bone formation marker PINP and the bone resorption marker CTX-I were lowest in the combination treatment group and markedly decreased compared with vehicle group. Concurrent administration of enzalutamide did not impair radium-223 uptake in tumor-bearing bone or the ability of radium-223 to inhibit tumor-induced abnormal bone formation. In conclusion, combination treatment with radium-223 and enzalutamide demonstrated enhanced antitumor efficacy without compromising the integrity of healthy bone. The results support the ongoing phase 3 trial of this combination. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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13 pages, 3175 KiB  
Article
Enhanced Succinate Oxidation with Mitochondrial Complex II Reactive Oxygen Species Generation in Human Prostate Cancer
by Aijun Zhang, Anisha A. Gupte, Somik Chatterjee, Shumin Li, Alberto G. Ayala, Brian J. Miles and Dale J. Hamilton
Int. J. Mol. Sci. 2022, 23(20), 12168; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012168 - 12 Oct 2022
Cited by 2 | Viewed by 1832
Abstract
The transformation of prostatic epithelial cells to prostate cancer (PCa) has been characterized as a transition from citrate secretion to citrate oxidation, from which one would anticipate enhanced mitochondrial complex I (CI) respiratory flux. Molecular mechanisms for this transformation are attributed to declining [...] Read more.
The transformation of prostatic epithelial cells to prostate cancer (PCa) has been characterized as a transition from citrate secretion to citrate oxidation, from which one would anticipate enhanced mitochondrial complex I (CI) respiratory flux. Molecular mechanisms for this transformation are attributed to declining mitochondrial zinc concentrations. The unique metabolic properties of PCa cells have become a hot research area. Several publications have provided indirect evidence based on investigations using pre-clinical models, established cell lines, and fixed or frozen tissue bank samples. However, confirmatory respiratory analysis on fresh human tissue has been hampered by multiple difficulties. Thus, few mitochondrial respiratory assessments of freshly procured human PCa tissue have been published on this question. Our objective is to document relative mitochondrial CI and complex II (CII) convergent electron flow to the Q-junction and to identify electron transport system (ETS) alterations in fresh PCa tissue. The results document a CII succinate: quinone oxidoreductase (SQR) dominant succinate oxidative flux model in the fresh non-malignant prostate tissue, which is enhanced in malignant tissue. CI NADH: ubiquinone oxidoreductase activity is impaired rather than predominant in high-grade malignant fresh prostate tissue. Given these novel findings, succinate and CII are promising targets for treating and preventing PCa. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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Review

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17 pages, 1045 KiB  
Review
Cardiovascular Complications in Patients with Prostate Cancer: Potential Molecular Connections
by Sooraj Kakkat, Paramahansa Pramanik, Seema Singh, Ajay Pratap Singh, Chandrani Sarkar and Debanjan Chakroborty
Int. J. Mol. Sci. 2023, 24(8), 6984; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24086984 - 10 Apr 2023
Cited by 5 | Viewed by 2880
Abstract
Cardiovascular diseases (CVDs) and complications are often seen in patients with prostate cancer (PCa) and affect their clinical management. Despite acceptable safety profiles and patient compliance, androgen deprivation therapy (ADT), the mainstay of PCa treatment and chemotherapy, has increased cardiovascular risks and metabolic [...] Read more.
Cardiovascular diseases (CVDs) and complications are often seen in patients with prostate cancer (PCa) and affect their clinical management. Despite acceptable safety profiles and patient compliance, androgen deprivation therapy (ADT), the mainstay of PCa treatment and chemotherapy, has increased cardiovascular risks and metabolic syndromes in patients. A growing body of evidence also suggests that patients with pre-existing cardiovascular conditions show an increased incidence of PCa and present with fatal forms of the disease. Therefore, it is possible that a molecular link exists between the two diseases, which has not yet been unraveled. This article provides insight into the connection between PCa and CVDs. In this context, we present our findings linking PCa progression with patients’ cardiovascular health by performing a comprehensive gene expression study, gene set enrichment (GSEA) and biological pathway analysis using publicly available data extracted from patients with advanced metastatic PCa. We also discuss the common androgen deprivation strategies and CVDs most frequently reported in PCa patients and present evidence from various clinical trials that suggest that therapy induces CVD in PCa patients. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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18 pages, 754 KiB  
Review
AR and PI3K/AKT in Prostate Cancer: A Tale of Two Interconnected Pathways
by Elisabetta Tortorella, Sabrina Giantulli, Alessandro Sciarra and Ida Silvestri
Int. J. Mol. Sci. 2023, 24(3), 2046; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032046 - 20 Jan 2023
Cited by 12 | Viewed by 4349
Abstract
Prostate cancer (PCa) is the most common cancer in men. The androgen receptor (AR) has a pivotal role in the pathogenesis and progression of PCa. Many therapies targeting AR signaling have been developed over the years. AR signaling inhibitors (ARSIs), including androgen synthesis [...] Read more.
Prostate cancer (PCa) is the most common cancer in men. The androgen receptor (AR) has a pivotal role in the pathogenesis and progression of PCa. Many therapies targeting AR signaling have been developed over the years. AR signaling inhibitors (ARSIs), including androgen synthesis inhibitors and AR antagonists, have proven to be effective in castration-sensitive PCa (CSPC) and improve survival, but men with castration-resistant PCa (CRPC) continue to have a poor prognosis. Despite a good initial response, drug resistance develops in almost all patients with metastatic CRPC, and ARSIs are no longer effective. Several mechanisms confer resistance to ARSI and include AR mutations but also hyperactivation of other pathways, such as PI3K/AKT/mTOR. This pathway controls key cellular processes, including proliferation and tumor progression, and it is the most frequently deregulated pathway in human cancers. A significant interaction between AR and the PI3K/AKT/mTOR signaling pathway has been shown in PCa. This review centers on the current scene of different AR and PI3K signaling pathway inhibitors, either as monotherapy or in combination treatments in PCa, and the treatment outcomes involved in both preclinical and clinical trials. A PubMed-based literature search was conducted up to November 2022. The most relevant and recent articles were selected to provide essential information and current evidence on the crosstalk between AR and the PI3K signaling pathways. The ClinicalTrials.gov registry was used to report information about clinical studies and their results using the Advanced research tool, filtering for disease and target. Full article
(This article belongs to the Special Issue Prostate Cancer: Pathology, Pathobiology and Therapy)
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