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Molecular Research on Prostate Cancer
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Molecular Research on Prostate Cancer

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 May 2024) | Viewed by 994

Special Issue Editor

Dr. Yaser Gamallat

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
Interests: prostate cancer; genomics; transcriptome; tumor biomarkers; tumorigenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prostate cancer represents a significant global health challenge, with a demand for improved patient outcomes. Despite treatment strategy advancements, the molecular complexity of this disease remains a daunting hurdle. Understanding the molecular mechanism driving prostate cancer initiation, progression and therapeutic resistance is pivotal for developing precise and effective interventions. 

This Special Issue aims to consolidate the latest findings and perspectives on the molecular landscape of prostate cancer, genomic alterations, epigenetic modifications, signaling pathways and novel biomarkers. We aim to foster a collaborative platform for researchers to contribute transformative insights that can shape the future of prostate cancer management and provide a comprehensive overview of the latest breakthroughs in the field. Authors are invited to contribute research articles elucidating the molecular intricacies underlying prostate cancer, fostering a deeper comprehension that can shape relevant targeted therapies and precision medicine. 

Dr. Yaser Gamallat
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
  • molecular biology
  • genomics
  • biomarkers
  • signaling pathways
  • precision medicine
  • treatment resistance
  • epigenetics
  • therapeutic targets

Published Papers (2 papers)

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Research

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14 pages, 1958 KiB  
Article
Anticancer Effect of Hemin through ANO1 Inhibition in Human Prostate Cancer Cells
by So-Hyeon Park, Yechan Lee, Hyejin Jeon, Junghwan Park, Jieun Kim, Mincheol Kang and Wan Namkung
Int. J. Mol. Sci. 2024, 25(11), 6032; https://doi.org/10.3390/ijms25116032 - 30 May 2024
Abstract
Anoctamin1 (ANO1), a calcium-activated chloride channel, is overexpressed in a variety of cancer cells, including prostate cancer, and is involved in cancer cell proliferation, migration, and invasion. Inhibition of ANO1 in these cancer cells exhibits anticancer effects. In this study, we conducted a [...] Read more.
Anoctamin1 (ANO1), a calcium-activated chloride channel, is overexpressed in a variety of cancer cells, including prostate cancer, and is involved in cancer cell proliferation, migration, and invasion. Inhibition of ANO1 in these cancer cells exhibits anticancer effects. In this study, we conducted a screening to identify novel ANO1 inhibitors with anticancer effects using PC-3 human prostate carcinoma cells. Screening of 2978 approved and investigational drugs revealed that hemin is a novel ANO1 inhibitor with an IC50 value of 0.45 μM. Notably, hemin had no significant effect on intracellular calcium signaling and cystic fibrosis transmembrane conductance regulator (CFTR), a cyclic AMP (cAMP)-regulated chloride channel, and it showed a weak inhibitory effect on ANO2 at 3 μM, a concentration that completely inhibits ANO1. Interestingly, hemin also significantly decreased ANO1 protein levels and strongly inhibited the cell proliferation and migration of PC-3 cells in an ANO1-dependent manner. Furthermore, it strongly induced caspase-3 activation, PARP degradation, and apoptosis in PC-3 cells. These findings suggest that hemin possesses anticancer properties via ANO1 inhibition and could be considered for development as a novel treatment for prostate cancer. Full article
(This article belongs to the Special Issue Molecular Research on Prostate Cancer)

Review

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16 pages, 1196 KiB  
Review
Homologous Recombination Repair Deficiency in Metastatic Prostate Cancer: New Therapeutic Opportunities
by Claudia Piombino, Stefania Pipitone, Elena Tonni, Luciana Mastrodomenico, Marco Oltrecolli, Cyrielle Tchawa, Rossana Matranga, Sara Roccabruna, Elisa D’Agostino, Marta Pirola, Francesca Bacchelli, Cinzia Baldessari, Maria Cristina Baschieri, Massimo Dominici, Roberto Sabbatini and Maria Giuseppa Vitale
Int. J. Mol. Sci. 2024, 25(9), 4624; https://doi.org/10.3390/ijms25094624 - 24 Apr 2024
Viewed by 622
Abstract
More than 20% of metastatic prostate cancer carries genomic defects involving DNA damage repair pathways, mainly in homologous recombination repair-related genes. The recent approval of olaparib has paved the way to precision medicine for the treatment of metastatic prostate cancer with PARP inhibitors [...] Read more.
More than 20% of metastatic prostate cancer carries genomic defects involving DNA damage repair pathways, mainly in homologous recombination repair-related genes. The recent approval of olaparib has paved the way to precision medicine for the treatment of metastatic prostate cancer with PARP inhibitors in this subset of patients, especially in the case of BRCA1 or BRCA2 pathogenic/likely pathogenic variants. In face of this new therapeutic opportunity, many issues remain unsolved. This narrative review aims to describe the relationship between homologous recombination repair deficiency and prostate cancer, the techniques used to determine homologous recombination repair status in prostate cancer, the crosstalk between homologous recombination repair and the androgen receptor pathway, the current evidence on PARP inhibitors activity in metastatic prostate cancer also in homologous recombination repair-proficient tumors, as well as emerging mechanisms of resistance to PARP inhibitors. The possibility of combination therapies including a PARP inhibitor is an attractive option, and more robust data are awaited from ongoing phase II and phase III trials outlined in this manuscript. Full article
(This article belongs to the Special Issue Molecular Research on Prostate Cancer)
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