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Male Genitourinary Tumors: Molecular Mechanisms and Potential Therapeutic Targets

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: 25 July 2024 | Viewed by 588

Special Issue Editors


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Guest Editor
Urology and Andrology Unit, Andria Teaching Hospital, University of Foggia, Foggia, Italy
Interests: urology; urogenital diseases; surgery
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Pathology, University of Foggia School of Medicine, 71121 Foggia, Italy
Interests: genitourinary pathology; diagnostic biomarkers; prognostic/predictive biomarkers; digital pathology; emolymphopathology; bladder cancer; prostate cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Genitourinary (GU) tumors are common in men of all ages, with prostate cancer and bladder cancer ranking 1st and 4th among the most prevalent tumors worldwide, respectively. Clinically, GU tumors are heterogeneous diseases, carrying either an aggressive outcome with progression and/or metastasis, or an indolent clinical course with low mortality rates. Such heterogeneity is underlined by different genetic/epigenetic events resulting in the initial development and further progression of these tumors. Over the last decades, advances in molecular technologies provided an insight into the pathogenesis of GU tumors, and pointed out possible biomarkers to be used in order to stratify men whose risk to develop tumors with poor outcome and/or not responding to conventional therapeutic options is higher as compared to the general population. Furthermore, some of those biomarkers with prognostic/predictive potential may also play a role as potential therapeutic targets, in light of the recent development of targeted treatments, novel approaches and technologies, and improvements in conventional therapeutic options.  This Special Issue is dedicated to investigating and describing the molecular mechanisms of GU tumorigenesis, and to reporting on novel molecules which can be used as potential therapeutic targets, as well as to broadening the use of established biomarkers. Both reviews and research articles focusing on these topics, expecially those applying findings from basic biology and clinical trials to tools fulfiling unmet clinical needs are welcome.

Prof. Dr. Luigi Cormio
Dr. Francesca Sanguedolce
Guest Editors

Manuscript Submission Information

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Keywords

  • prostate cancer
  • bladder cancer
  • biomarkers
  • molecular mechanisms
  • therapeutic targets
  • translational research

Published Papers (1 paper)

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Research

11 pages, 14502 KiB  
Article
The Reduction of PSMB4 in T24 and J82 Bladder Cancer Cells Inhibits the Angiogenesis and Migration of Endothelial Cells
by Yi-Hsuan Lin, Tzu-Min Chen, Yu-Ling Tsai, Wen-Chiuan Tsai, Hisao-Hsien Wang, Ying Chen and Sheng-Tang Wu
Int. J. Mol. Sci. 2024, 25(10), 5559; https://doi.org/10.3390/ijms25105559 - 20 May 2024
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Abstract
Bladder cancer (BC) is a malignant tumor of the urinary system with high mortality and recurrence rates. Proteasome subunit type 4 (PSMB4) is highly expressed and has been identified as having oncogenic properties in a variety of cancer types. This study aimed to [...] Read more.
Bladder cancer (BC) is a malignant tumor of the urinary system with high mortality and recurrence rates. Proteasome subunit type 4 (PSMB4) is highly expressed and has been identified as having oncogenic properties in a variety of cancer types. This study aimed to explore the effect of PSMB4 knockdown on the survival, migration, and angiogenesis of human bladder cancer cells with different degrees of malignancy. We analyzed the effects of PSMB4 knockdown in bladder cancer cells and endothelial cells in the tumor microenvironment. PSMB4 was highly expressed in patients with low- and high-grade urothelial carcinoma. Inhibition of PSMB4 reduced protein expression of focal adhesion kinase (FAK) and myosin light chain (MLC), leading to reduced migration. Furthermore, the suppression of PSMB4 decreased the levels of vascular endothelial factor B (VEGF-B), resulting in lower angiogenic abilities in human bladder cancer cells. PSMB4 inhibition affected the migratory ability of HUVECs and reduced VEGFR2 expression, consequently downregulating angiogenesis. In the metastatic animal model, PSMB4 knockdown reduced the relative volumes of lung tumors. Our findings suggest the role of PSMB4 as a potential target for therapeutic strategies against human bladder cancer. Full article
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