Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Prostate Cancer: Signaling Pathways and Molecular Targets

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 12658

Share This Special Issue

Special Issue Editor

Dr. Manuel Scimeca

E-Mail Website
Guest Editor

Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133 Rome, Italy
Interests: environmental pollution; oncology; cardiovascular diseases; electron microscopy; histology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the era of 4P medicine (predictive, preventive, personalized and participatory), the identification of new reliable molecular targets for both diagnosis and treatment of prostate cancer represents one of the most interesting challenge of the scientific community. In fact, prostate cancer is the second leading cause of cancer death in men, behind only lung cancer.

Despite that the introduction of screening analysis such as Prostate Specific Antigen (PSA) Test and Digital Rectal Examination significantly increased the survival rate in prostate cancer patients, no molecular targets are currently available to predict the progress of prostate cancers and the relative risk to develop metastatic lesions. In addition, the use of targeted therapies available for prostate cancers (e.g., anti-PSMA inhibitors) are currently established only after the detection of molecular targets by invasive exams as histological examination. In this context, the identifications of molecular pathways involved in prostate cancer occurrence and progression, as well as the development of innovative in vitro, ex vivo and in vivo strategies capable to discover specific molecular targets represent the scientific rationale in support of tailored targeted therapies. In spite of these recent and promising pre-clinical discoveries, individually tailored medical care is still far from reality requiring synergistic, transdisciplinary competencies in the field of biomedicine. In this scenario, it appears evident that working towards personalized medicine in prostate oncology requires the synergic combination of several disciplines such as molecular biology, pathology and molecular medicine, which represent complementary approaches to investigate the fundamental mechanisms involved in prostate cancer.

Therefore, the combination of these disciplines in basic research, pre-clinical and clinical investigations can provide the scientific rationale to identify the main molecular pathways involved in prostate cancer through which to “enlighten” the way towards the personalized medicine.

Starting from these considerations, the aim of this Special Issue is to publish the latest discoveries and bring together researchers and clinicians working in the field of Prostate Cancer.

Topics will include (but are not limited to) the following:

Identification of new molecular pathways involved in prostate cancer progression
Characterization of prostate cancer metastatic cells
Potential targets for personalized medicine
Potential targets for theragnostic approaches
Identification of novel in situ prostate cancer biomarkers
Prostate cancer circulating cells
Identification and development of reliable molecular imaging molecules
Molecular-targeted therapies in prostate cancer
Innovative and in vitro and pre-clinical strategies to discover specific molecular targets

Dr. Manuel Scimeca
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

urinary biomarkers on prostate cancer
serum/plasma biomarkers
tissue biomarkers (nuleic acid/protein-based)
multivariate models
immunoregulation, molecular signal
cells grow and spread
apoptosis
transcription

Published Papers (4 papers)

Download All Papers

Research

Jump to: Review

16 pages, 2312 KiB

Open AccessArticle

Pro-Survival Factor EDEM3 Confers Therapy Resistance in Prostate Cancer

by Emma Scott, Rebecca Garnham, Kathleen Cheung, Adam Duxfield, David J. Elliott and Jennifer Munkley

Int. J. Mol. Sci. 2022, 23(15), 8184; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158184 - 25 Jul 2022

Cited by 4 | Viewed by 1957

Abstract

Prostate cancer is the most common cancer in men, and it is primarily driven by androgen steroid hormones. The glycosylation enzyme EDEM3 is controlled by androgen signalling and is important for prostate cancer viability. EDEM3 is a mannosidase that trims mannose from mis-folded glycoproteins, tagging them for degradation through endoplasmic reticulum-associated degradation. Here, we find that EDEM3 is upregulated in prostate cancer, and this is linked to poorer disease-free survival. Depletion of EDEM3 from prostate cancer cells induces an ER stress transcriptomic signature, and EDEM3 overexpression is cyto-protective against ER stressors. EDEM3 expression also positively correlates with genes involved in the unfolded protein response in prostate cancer patients, and its expression can be induced through exposure to radiation. Importantly, the overexpression of EDEM3 promotes radio-resistance in prostate cancer cells and radio-resistance can be reduced through depletion of EDEM3. Our data thus implicate increased levels of EDEM3 with a role in prostate cancer pathology and reveal a new therapeutic opportunity to sensitise prostate tumours to radiotherapy. Full article

(This article belongs to the Special Issue Prostate Cancer: Signaling Pathways and Molecular Targets)

► Show Figures

Figure 1

15 pages, 19492 KiB

Open AccessArticle

Overexpression of Nucleolin and Associated Genes in Prostate Cancer

by Virginie Firlej, Pascale Soyeux, Maya Nourieh, Eric Huet, Fannie Semprez, Yves Allory, Arturo Londono-Vallejo, Alexandre de la Taille, Francis Vacherot and Damien Destouches

Int. J. Mol. Sci. 2022, 23(9), 4491; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094491 - 19 Apr 2022

Cited by 6 | Viewed by 1893

Abstract

Prostate cancer (PCa) is the second most frequent cancer and the fifth leading cause of cancer death in men worldwide. If local PCa presents a favorable prognosis, available treatments for advanced PCa display limiting benefits due to therapeutic resistances. Nucleolin (NCL) is a ubiquitous protein involved in numerous cell processes, such as ribosome biogenesis, cell cycles, or angiogenesis. NCL is overexpressed in several tumor types in which it has been proposed as a diagnostic and prognostic biomarker. In PCa, NCL has mainly been studied as a target for new therapeutic agents. Nevertheless, little data are available concerning its expression in patient tissues. Here, we investigated the expression of NCL using a new cohort from Mondor Hospital and data from published cohorts. Results were then compared with NCL expression using in vitro models. NCL was overexpressed in PCa tissues compared to the normal tissues, but no prognostic values were demonstrated. Nine genes were highly co-expressed with NCL in patient tissues and tumor prostate cell lines. Our data demonstrate that NCL is an interesting diagnostic biomarker and propose a signature of genes co-expressed with NCL. Full article

(This article belongs to the Special Issue Prostate Cancer: Signaling Pathways and Molecular Targets)

► Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1500 KiB

Open AccessReview

Targeting Mitochondrial OXPHOS and Their Regulatory Signals in Prostate Cancers

by Chia-Lin Chen, Ching-Yu Lin and Hsing-Jien Kung

Int. J. Mol. Sci. 2021, 22(24), 13435; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413435 - 14 Dec 2021

Cited by 16 | Viewed by 4703

Abstract

Increasing evidence suggests that tumor development requires not only oncogene/tumor suppressor mutations to drive the growth, survival, and metastasis but also metabolic adaptations to meet the increasing energy demand for rapid cellular expansion and to cope with the often nutritional and oxygen-deprived microenvironment. One well-recognized strategy is to shift the metabolic flow from oxidative phosphorylation (OXPHOS) or respiration in mitochondria to glycolysis or fermentation in cytosol, known as Warburg effects. However, not all cancer cells follow this paradigm. In the development of prostate cancer, OXPHOS actually increases as compared to normal prostate tissue. This is because normal prostate epithelial cells divert citrate in mitochondria for the TCA cycle to the cytosol for secretion into seminal fluid. The sustained level of OXPHOS in primary tumors persists in progression to an advanced stage. As such, targeting OXPHOS and mitochondrial activities in general present therapeutic opportunities. In this review, we summarize the recent findings of the key regulators of the OXPHOS pathway in prostate cancer, ranging from transcriptional regulation, metabolic regulation to genetic regulation. Moreover, we provided a comprehensive update of the current status of OXPHOS inhibitors for prostate cancer therapy. A challenge of developing OXPHOS inhibitors is to selectively target cancer mitochondria and spare normal counterparts, which is also discussed. Full article

(This article belongs to the Special Issue Prostate Cancer: Signaling Pathways and Molecular Targets)

► Show Figures

Figure 1

10 pages, 798 KiB

Open AccessReview

FOXO3a and Its Regulators in Prostate Cancer

by Dominika Ewa Habrowska-Górczyńska, Marta Justyna Kozieł, Karolina Kowalska and Agnieszka Wanda Piastowska-Ciesielska

Int. J. Mol. Sci. 2021, 22(22), 12530; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212530 - 20 Nov 2021

Cited by 19 | Viewed by 3112

Abstract

Forkhead box O3 (FOXO3a) is a member of a subfamily of forkhead transcription factors involved in the basic processes within a cell, including proliferation, apoptosis, cell cycle regulation, and DNA damage. As a transcription factor, FOXO3a is involved in the response to cellular stress, UV radiation, or oxidative stress. Its regulation is based on the modification of proteins as well as regulation by other proteins, e.g., growth factors. FOXO3a is commonly deregulated in cancer cells, and its inactivation is associated with initiation and progression of tumorigenesis, suggesting its role as a tumor suppressor; however, its role is still disputed and seems to be dependent on upstream signaling. Nevertheless, FOXO3a serves as an interesting potential target in therapies as it is regulated during treatment with very common anti-cancer drugs such as paclitaxel, cisplatin, docetaxel, and doxorubicin. This review aims to update the reported role of FOXO3a in prostate cancer (PCa), with a focus on its regulators that might serve as potential therapeutic agents in PCa therapy. Full article

(This article belongs to the Special Issue Prostate Cancer: Signaling Pathways and Molecular Targets)

► Show Figures