International Journal of Molecular Sciences

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Emerging Biological Markers and Molecular Targets in Bladder Cancer

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Dr. Stanislav Žiaran

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Department of Urology, Faculty of Medicine, Comenius University in Bratislava, Ružinovská 6, 826 06 Bratislava, Slovakia
Interests: urologic oncology; bladder cancer; tissue engineering; regenerative urology; molecular biomarkers; extracellular matrix biology; decellularization and recellularization; translational medicine; precision diagnostics
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Dear Colleagues,

Bladder cancer remains one of the most prevalent malignancies of the urinary tract, marked by high recurrence rates, molecular heterogeneity, and a complex tumor microenvironment. The discovery and validation of novel biological markers hold great promise for advancing diagnosis, prognosis, and personalized therapeutic strategies.

This Special Issue aims to highlight cutting-edge research on molecular and cellular biomarkers, genetic and epigenetic alterations, liquid biopsy techniques, and emerging therapeutic targets relevant to urothelial carcinoma. Studies employing multi-omics approaches, bioinformatics, AI-driven analytics, and translational or clinical models are particularly encouraged.

We welcome original research articles, systematic reviews, and comprehensive overviews that address emerging trends in biomarker discovery, validation, and clinical implementation in bladder cancer.

We warmly invite you to contribute your latest findings to this Special Issue.

Dr. Stanislav Žiaran
Guest Editor

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16 pages, 8923 KB

Open AccessArticle

HCN2 Promotes BGN Transcription via REST to Regulate Ferroptosis and Tumor Progression in Bladder Cancer

by Yudong Cao, Jinchao Ma, Xingxing Tang, Yushuang Cui, Xiao Yang, Yongpeng Ji, Ruijian You, Chen Lin, Shuo Wang and Peng Du

Int. J. Mol. Sci. 2026, 27(8), 3433; https://doi.org/10.3390/ijms27083433 - 11 Apr 2026

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Abstract

Bladder cancer is one of the most common malignancies of the urinary system. Identifying new potential therapeutic targets and exploring molecular mechanisms are crucial for improving treatment and prognosis. The hyperpolarization-activated cyclic nucleotide-gated (HCN) channel 2, known to play a key role in various physiological and pathological processes, has an unclear function and mechanism of action in bladder cancer. We employed bioinformatics analysis and immunohistochemistry to assess the role of HCN2 in bladder cancer, integrating in vitro and in vivo models to evaluate the impact of HCN2 on cell behavior. Molecular interactions were characterized using immunoprecipitation, chromatin immunoprecipitation, and dual-luciferase reporter assays. Our investigation revealed a significant upregulation of HCN2 in bladder cancer tissues, which was predictive of a poorer clinical outcome. Functionally, HCN2 knockdown in bladder cancer impeded cell proliferation, induced apoptosis, and curtailed migration and invasion. Mechanistically, the overexpression of HCN2 contributed to the translocation of the REST transcription factor into the nucleus and facilitated its binding to the BGN promoter for transcriptional activation of its expression. This regulatory mechanism was shown to suppress ferroptosis, a form of regulated cell death, thereby enhancing the proliferative and tumorigenesis of bladder cancer cells. This study uncovers the novel mechanism by which HCN2 regulates ferroptosis via the REST-BGN axis, affecting bladder cancer cell behavior, and provides new perspectives and strategies for future clinical treatment. Full article

(This article belongs to the Special Issue Emerging Biological Markers and Molecular Targets in Bladder Cancer)

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25 pages, 16752 KB

Open AccessReview

FGFR3 Alterations and Nectin-4 Expression as Therapeutic Biomarkers in Bladder Cancer: A Systematic Review and Single-Arm Meta-Analysis

by Petar Antonov, Gabriela Raycheva, Denis Eshrefov, Angel Belov, Petar Uchikov, Atanas Ivanov, Veselin Popov, Matteo Pacini, Alessandro Zucchi, Andrea Nicolini and Plamen Penchev

Int. J. Mol. Sci. 2026, 27(11), 5007; https://doi.org/10.3390/ijms27115007 - 1 Jun 2026

Viewed by 1134

Abstract

Bladder cancer is a molecularly heterogeneous malignancy in which biomarker-driven therapies increasingly shape clinical management. Fibroblast growth factor receptor 3 (FGFR3) alterations and nectin-4 expression are key therapeutic targets, yet their integrated biological and clinical relevance remains unclear. A systematic search of PubMed, Scopus, and Cochrane Central was conducted from database inception to 22 February 2026 (PROSPERO: CRD420261309413). Studies reporting the prevalence of FGFR3 alterations and/or nectin-4 expression in bladder cancer were included. Proportions were pooled using a random-effects model with restricted maximum likelihood and Freeman–Tukey transformation. Heterogeneity was assessed with I² and Cochran’s Q. Fourteen studies (three randomized and 11 observational), including 3955 patients (mean age: 67.34 years), were analyzed. The pooled prevalence of FGFR3 alterations was 52% (95% CI: 23.33–80.12; I² = 99%), while that of nectin-4 expression was 78% (95% CI: 64.23–89.81; I² = 91%). FGFR3 prevalence varied significantly by disease stage, study design, and region, with higher rates in advanced/metastatic disease and randomized trials (p < 0.05). Nectin-4 expression was generally high across included studies, although interpretation was limited by the small number of studies and assay variability. Sensitivity analyses showed the stability of estimates; however, interpretation is limited by substantial heterogeneity. The observed prevalence estimates are strongly influenced by study design, biomarker selection, and assay variability, limiting their interpretation as true biological prevalence. These results should, therefore, be interpreted cautiously and viewed as descriptive rather than definitive estimates. Separate analyses of biomarker-enriched trials and unselected cohorts are necessary to obtain clinically meaningful estimates. Full article

(This article belongs to the Special Issue Emerging Biological Markers and Molecular Targets in Bladder Cancer)

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