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Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers

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 (15 April 2023) | Viewed by 11149

Special Issue Editor

Prof. Dr. Masatoshi Watanabe

E-Mail Website
Guest Editor
Department of Oncologic Pathology, Graduate School of Medicine, Mie University, Tsu 514-8507, Mie, Japan
Interests: prostate cancer; tumor microenvironment; organelle; medical engineering
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prostate cancer (PC) is the second most frequently diagnosed cancer and the fifth leading cause of cancer death among men worldwide. The diagnosis and treatments of prostate cancer continue to evolve rapidly, based on the understanding of the genomic landscape and biology of prostate cancer. Under these circumstances, identifying the effective biomarkers for prognosis and therapeutics became a major focus, leading to the improvement of outcomes and selection of patient-specific therapeutics. High-risk prostate cancer has been defined by a patient’s Gleason score, PSA level, and clinical T stage; however, a novel marker is needed. Recently, the presence of intraductal carcinoma of the prostate has been considered to be important based on clinic–pathological and/or genetic analysis. This Special Issue focuses on “Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers”, including the potential new markers based on pathology or molecular biology.

We welcome submissions including research articles and review articles on the widely discussed topics.

Prof. Dr. Masatoshi Watanabe
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.

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Keywords

  • Pathological markers for Prostate Cancers
  • Molecular markers for Prostate Cancers
  • Candidate markers for Prostate Cancers
  • Tumor microenvironment
  • Epigenetics
  • metabolism
  • signaling
  • receptor
  • nanomedicine
  • genomics

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Published Papers (4 papers)

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Research

15 pages, 2687 KiB  
Article
Multi-Gene Next-Generation Sequencing Panel for Analysis of BRCA1/BRCA2 and Homologous Recombination Repair Genes Alterations Metastatic Castration-Resistant Prostate Cancer
by Thais Maloberti, Antonio De Leo, Sara Coluccelli, Viviana Sanza, Elisa Gruppioni, Annalisa Altimari, Stefano Zagnoni, Francesca Giunchi, Francesco Vasuri, Michelangelo Fiorentino, Veronica Mollica, Simona Ferrari, Sara Miccoli, Michela Visani, Daniela Turchetti, Francesco Massari, Giovanni Tallini and Dario de Biase
Int. J. Mol. Sci. 2023, 24(10), 8940; https://doi.org/10.3390/ijms24108940 - 18 May 2023
Cited by 5 | Viewed by 2548
Abstract
Despite significant therapeutic advances, metastatic CRPC (mCRPC) remains a lethal disease. Mutations in homologous recombination repair (HRR) genes are frequent in mCRPC, and tumors harboring these mutations are known to be sensitive to PARP inhibitors. The aim of this study was to verify [...] Read more.
Despite significant therapeutic advances, metastatic CRPC (mCRPC) remains a lethal disease. Mutations in homologous recombination repair (HRR) genes are frequent in mCRPC, and tumors harboring these mutations are known to be sensitive to PARP inhibitors. The aim of this study was to verify the technical effectiveness of this panel in the analysis of mCRPC, the frequency and type of mutations in the BRCA1/BRCA2 genes, as well as in the homologous recombination repair (HRR) genes. A total of 50 mCRPC cases were analyzed using a multi-gene next-generation sequencing panel evaluating a total of 1360 amplicons in 24 HRR genes. Of the 50 cases, 23 specimens (46.0%) had an mCRPC harboring a pathogenic variant or a variant of uncertain significance (VUS), whereas in 27 mCRPCs (54.0%), no mutations were detected (wild-type tumors). BRCA2 was the most commonly mutated gene (14.0% of samples), followed by ATM (12.0%), and BRCA1 (6.0%). In conclusion, we have set up an NGS multi-gene panel that is capable of analyzing BRCA1/BRCA2 and HRR alterations in mCRPC. Moreover, our clinical algorithm is currently being used in clinical practice for the management of patients with mCRPC. Full article
(This article belongs to the Special Issue Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers)
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14 pages, 4383 KiB  
Article
Downregulation of BUD31 Promotes Prostate Cancer Cell Proliferation and Migration via Activation of p-AKT and Vimentin In Vitro
by Muhammad Choudhry, Yaser Gamallat, Ealia Khosh Kish, Sima Seyedi, Geoffrey Gotto, Sunita Ghosh and Tarek A. Bismar
Int. J. Mol. Sci. 2023, 24(7), 6055; https://doi.org/10.3390/ijms24076055 - 23 Mar 2023
Cited by 4 | Viewed by 2218
Abstract
Among men, prostate cancer (PCa) is the second most frequently diagnosed cancer subtype and has demonstrated a high degree of prevalence globally. BUD31, also known as Functional Spliceosome-Associated Protein 17, is a protein that works at the level of the spliceosome; it is [...] Read more.
Among men, prostate cancer (PCa) is the second most frequently diagnosed cancer subtype and has demonstrated a high degree of prevalence globally. BUD31, also known as Functional Spliceosome-Associated Protein 17, is a protein that works at the level of the spliceosome; it is functionally implicated in pre-mRNA splicing as well as processing, while also acting as a transcriptional regulator of androgen receptor (AR) target genes. Clinically, the expression of BUD31 and its functions in the development and progression of PCa is yet to be elucidated. The BUD31 expression was assessed using IHC in a tissue microarray (TMA) constructed from a cohort of 284 patient samples. In addition, we analyzed the prostate adenocarcinoma (TCGAPRAD-) database. Finally, we used PCa cell lines to knockdown BUD31 to study the underlying mechanisms in vitro.Assesment of BUD31 protein expression revealed lower expression in incidental and advanced PCa, and significantly lower expression was observed in patients diagnosed with castrate-resistant prostate cancer. Additionally, bioinformatic analysis and GSEA revealed that BUD31 increased processes related to cancer cell migration and proliferation. In vitro results made evident that BUD31 knockdown in PC3 cells led to an increase in the G2 cell population, indicating a more active and proliferative state. Additionally, an investigation of metastatic processes revealed that knockdown of BUD31 significantly enhanced the ability of PC3 cells to migrate and invade. Our in vitro results showed BUD31 knockdown promotes cell proliferation and migration of prostate cancer cells via activation of p-AKT and vimentin. These results support the clinical data, where low expression of BUD31 was correlated to more advanced stages of PCa. Full article
(This article belongs to the Special Issue Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers)
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17 pages, 7082 KiB  
Article
Glycyl-tRNA Synthetase (GARS) Expression Is Associated with Prostate Cancer Progression and Its Inhibition Decreases Migration, and Invasion In Vitro
by Ealia Khosh Kish, Yaser Gamallat, Muhammad Choudhry, Sunita Ghosh, Sima Seyedi and Tarek A. Bismar
Int. J. Mol. Sci. 2023, 24(5), 4260; https://doi.org/10.3390/ijms24054260 - 21 Feb 2023
Cited by 5 | Viewed by 2679
Abstract
Glycyl-tRNA synthetase (GARS) is a potential oncogene associated with poor overall survival in various cancers. However, its role in prostate cancer (PCa) has not been investigated. Protein expression of GARS was investigated in benign, incidental, advanced, and castrate-resistant PCa (CRPC) patient samples. We [...] Read more.
Glycyl-tRNA synthetase (GARS) is a potential oncogene associated with poor overall survival in various cancers. However, its role in prostate cancer (PCa) has not been investigated. Protein expression of GARS was investigated in benign, incidental, advanced, and castrate-resistant PCa (CRPC) patient samples. We also investigated the role of GARS in vitro and validated GARS clinical outcomes and its underlying mechanism, utilizing The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA PRAD) database. Our data revealed a significant association between GARS protein expression and Gleason groups. Knockdown of GARS in PC3 cell lines attenuated cell migration and invasion and resulted in early apoptosis signs and cellular arrest in S phase. Bioinformatically, higher GARS expression was observed in TCGA PRAD cohort, and there was significant association with higher Gleason groups, pathological stage, and lymph nodes metastasis. High GARS expression was also significantly correlated with high-risk genomic aberrations such as PTEN, TP53, FXA1, IDH1, SPOP mutations, and ERG, ETV1, and ETV4 gene fusions. Gene Set Enrichment Analysis (GSEA) of GARS through the TCGA PRAD database provided evidence for upregulation of biological processes such as cellular proliferation. Our findings support the oncogenic role of GARS involved in cellular proliferation and poor clinical outcome and provide further evidence for its use as a potential biomarker in PCa. Full article
(This article belongs to the Special Issue Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers)
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18 pages, 3342 KiB  
Article
Androgen Deprivation Freezes Hormone-Sensitive Prostate Cancer Cells in a Reversible, Genetically Unstable Quasi-Apoptotic State, Bursting into Full Apoptosis upon Poly(ADP-ribose) Polymerase Inhibition
by Andrea Pelliccia, Francesco Capradossi, Francesca Corsi, Greta Deidda Tarquini, Emanuele Bruni, Albrecht Reichle, Francesco Torino and Lina Ghibelli
Int. J. Mol. Sci. 2023, 24(3), 2040; https://doi.org/10.3390/ijms24032040 - 20 Jan 2023
Cited by 2 | Viewed by 2946
Abstract
Androgen deprivation therapy (ADT) is a powerful treatment for metastatic hormone-sensitive prostate cancer (mHSPC) patients, but eventually and inevitably, cancer relapses, progressing to the fatal castration-resistant (CR)PC stage. Progression implies the emergence of cells proliferating in the absence of androgen through still elusive [...] Read more.
Androgen deprivation therapy (ADT) is a powerful treatment for metastatic hormone-sensitive prostate cancer (mHSPC) patients, but eventually and inevitably, cancer relapses, progressing to the fatal castration-resistant (CR)PC stage. Progression implies the emergence of cells proliferating in the absence of androgen through still elusive mechanisms. We show here for the first time that ADT induces LNCaP mHSPC cells to collectively enter a metastable quasi-apoptotic state (QUAPS) consisting of partial mitochondrial permeabilization, limited BAX and caspase activation, and moderate induction of caspase-dependent dsDNA breaks; despite this, cells maintain full viability. QUAPS is destabilized by poly(ADP)-polymerase inhibition (PARPi), breaking off toward overt intrinsic apoptosis and culture extinction. Instead, QUAPS is rapidly and efficiently reverted upon androgen restoration, with mitochondria rapidly recovering integrity and cells collectively resuming normal proliferation. Notably, replication restarts before DNA repair is completed, and implies an increased micronuclei frequency, indicating that ADT promotes genetic instability. The recovered cells re-acquire insensitivity to PARPi (as untreated LNCaP), pointing to specific, context-dependent vulnerability of mHSPC cells to PARPi during ADT. Summarizing, QUAPS is an unstable, pro-mutagenic state developing as a pro-survival pathway stabilized by PARP, and constitutes a novel viewpoint explaining how ADT-treated mHSPC may progress to CRPC, indicating possible preventive countermeasures. Full article
(This article belongs to the Special Issue Pathological and Molecular Markers for Diagnosis, Prognostic and Therapeutics of Prostate Cancers)
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