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Urologic Cancers: Molecular Basis for Novel Therapeutic Approaches
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Urologic Cancers: Molecular Basis for Novel Therapeutic Approaches

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: 31 December 2025 | Viewed by 3461

Special Issue Editor

Dr. Whi-An Kwon

E-Mail Website
Guest Editor
Department of Urology, Myongji Hospital, Hanyang University College of Medicine, 55, Hwasu-ro 14 beon-gil, Deogyang-gu, Gyeonggi-do, Goyang-si 10475, Republic of Korea
Interests: urothelial cancer; urologic oncology; medical oncology; drug development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Urologic cancers remain a globally significant health burden. Among these, prostate cancer, urothelial carcinoma, and renal cell carcinoma illustrate the complexity and heterogeneity of disease biology. Advances in genomics, epigenomics, and proteomics have deepened our understanding of tumor initiation, progression, and resistance. These molecular insights have paved the way for novel therapeutics, including targeted small-molecule inhibitors and immunotherapies, which have demonstrated considerable promise in both early and advanced disease settings. Emerging biomarkers, such as circulating tumor DNA and genomic signatures, hold potential to refine risk stratification and inform personalized treatment strategies. New diagnostic methods, such as liquid biopsies and artificial intelligence-driven imaging, complement these tailored approaches by enabling more accurate disease monitoring. Ultimately, unraveling the intricate molecular pathways behind these malignancies is crucial for the design of next-generation therapies, positioning the molecular basis as the central driving force to further elevate patient outcomes and long-term survival in clinical urologic oncology. We welcome original research, and comprehensive reviews that provide insights into these emerging innovations in urologic oncology.

Dr. Whi-An Kwon
Guest Editor

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Keywords

  • urologic cancers
  • prostate cancer
  • urothelial cancer
  • renal cell cancer
  • genomics
  • proteomics
  • biomarkers
  • molecular pathways

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Published Papers (3 papers)

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Research

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19 pages, 10627 KB  
Article
Novel Therapeutic Strategy for Renal Cell Carcinoma: Niclosamide Enhances Sunitinib Efficacy via DNA Repair and Cell Cycle Pathways
by Ae Ryang Jung, Ga Eun Kim, Mee Young Kim, Seung Ah Rhew, Dongho Shin, U-Syn Ha, Sung-Hoo Hong, Ji Youl Lee, Sae Woong Kim and Yong Hyun Park
Int. J. Mol. Sci. 2025, 26(22), 10922; https://doi.org/10.3390/ijms262210922 - 11 Nov 2025
Viewed by 409
Abstract
Tyrosine kinase inhibitors (TKIs), such as sunitinib and sorafenib, are standard treatments for renal cell carcinoma (RCC). However, most patients treated with these drugs eventually develop drug resistance and relapse; therefore, new treatment options for RCC are urgently required. Recent studies have focused [...] Read more.
Tyrosine kinase inhibitors (TKIs), such as sunitinib and sorafenib, are standard treatments for renal cell carcinoma (RCC). However, most patients treated with these drugs eventually develop drug resistance and relapse; therefore, new treatment options for RCC are urgently required. Recent studies have focused on combination therapies targeting distinct molecular pathways that may produce synergistic effects and help overcome drug resistance in RCC. Niclosamide, an anthelmintic agent, is effective against various cancers; however, its potential in combination with sunitinib for treating RCC has not been evaluated. In this study, we assessed the therapeutic efficacy of niclosamide in combination with sunitinib against RCC and explored the underlying molecular mechanisms. Niclosamide alone inhibited RCC cell proliferation, whereas its combination with sunitinib produced a synergistic anticancer effect, both in vitro and in vivo. RNA sequencing (RNA-seq) and bioinformatic analyses showed that niclosamide modulated critical pathways, including BRIP1- and FANCA-mediated DNA repair and E2F2-regulated cell cycle progression. These findings provide proof-of-concept that niclosamide enhances TKI efficacy through modulation of DNA repair and cell cycle pathways, supporting the rationale for DNA damage response (DDR)-targeted combination strategies in RCC. Full article
(This article belongs to the Special Issue Urologic Cancers: Molecular Basis for Novel Therapeutic Approaches)
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28 pages, 3757 KB  
Article
Growth Hormone Signaling in Bladder Cancer: Transcriptomic Profiling of Patient Samples and In Vitro Evidence of Therapy Resistance via ABC Transporters and EMT Activation
by Emily Davis, Lydia J. Caggiano, Hannah Munholland, Reetobrata Basu, Darlene E. Berryman and John J. Kopchick
Int. J. Mol. Sci. 2025, 26(15), 7113; https://doi.org/10.3390/ijms26157113 - 23 Jul 2025
Viewed by 1455
Abstract
Growth hormone (GH) signaling has been implicated in tumor progression and therapy resistance across multiple cancer types, yet its role in bladder cancer remains largely unexplored. In this study, we investigated the impact of GH and its receptor (GHR) on therapy resistance and [...] Read more.
Growth hormone (GH) signaling has been implicated in tumor progression and therapy resistance across multiple cancer types, yet its role in bladder cancer remains largely unexplored. In this study, we investigated the impact of GH and its receptor (GHR) on therapy resistance and disease progression in urothelial carcinoma (UC) through integrated transcriptomic and in vitro analyses. Transcriptomic profiling of The Cancer Genome Atlas bladder cancer cohort revealed that high tumoral GHR expression was associated with differential upregulation of genes involved in drug efflux, epithelial-to-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. Notably, elevated GHR levels correlated with significantly reduced overall survival in patients with UC. In parallel, in vitro experiments demonstrated that GH promotes chemoresistance in UC cell lines via upregulation of ATP-binding cassette-containing (ABC) transporters and activation of EMT. GH also modulated ECM-remodeling-associated genes in a chemotherapy-dependent manner, including matrix metalloproteinases and tissue inhibitors of metalloproteinases. Importantly, these effects were abrogated by Pegvisomant, a GHR antagonist, indicating the functional relevance of GH/GHR signaling in the mediation of these phenotypes. Collectively, our findings support a mechanistic role for GH signaling in driving therapy resistance and tumor aggressiveness in bladder cancer and suggest GHR antagonism as a potential therapeutic strategy to improve treatment outcomes. Full article
(This article belongs to the Special Issue Urologic Cancers: Molecular Basis for Novel Therapeutic Approaches)
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Review

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23 pages, 2776 KB  
Review
Nuclear Receptors in Bladder Cancer: Insights into miRNA-Mediated Regulation and Potential Therapeutic Implications
by José Javier Flores-Estrada, Adriana Jiménez, Georgina Victoria-Acosta, Enoc Mariano Cortés-Malagón, María Guadalupe Ortiz-López, María Elizbeth Alvarez-Sánchez, Stephanie I. Nuñez-Olvera, Yussel Fernando Pérez-Navarro, Marcos Morales-Reyna and Jonathan Puente-Rivera
Int. J. Mol. Sci. 2025, 26(15), 7340; https://doi.org/10.3390/ijms26157340 - 29 Jul 2025
Viewed by 1220
Abstract
Nuclear receptors (NRs) are ligand-activated transcription factors that regulate gene expression and are involved in diverse physiological and pathological processes, including carcinogenesis. In bladder cancer (BCa), dysregulation of NR signaling pathways has been linked to tumor initiation, progression, therapy resistance, and immune evasion. [...] Read more.
Nuclear receptors (NRs) are ligand-activated transcription factors that regulate gene expression and are involved in diverse physiological and pathological processes, including carcinogenesis. In bladder cancer (BCa), dysregulation of NR signaling pathways has been linked to tumor initiation, progression, therapy resistance, and immune evasion. Recent evidence highlights the intricate crosstalk between NRs and microRNAs (miRNAs), which are small non-coding RNAs that posttranscriptionally modulate gene expression. This review provides an integrated overview of the molecular interactions between key NRs and miRNAs in BCa. We investigated how miRNAs regulate NR expression and function and, conversely, how NRs influence miRNA biogenesis, thereby forming regulatory feedback loops that shape tumor behavior. Specific miRNA–NR interactions affecting epithelial-to-mesenchymal transition, metabolic reprogramming, angiogenesis, and chemoresistance are discussed in detail. Additionally, we highlight therapeutic strategies targeting NR–miRNA networks, including selective NR modulators, miRNA mimics and inhibitors, as well as RNA-based combinatorial approaches focusing on their utility as diagnostic biomarkers and personalized treatment targets. Understanding the molecular complexity of NR–miRNA regulation in BCa may open new avenues for improving therapeutic outcomes and advancing precision oncology in urological cancers. Full article
(This article belongs to the Special Issue Urologic Cancers: Molecular Basis for Novel Therapeutic Approaches)
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