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Molecular Mechanisms of Bladder Cancer

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: 1 December 2026 | Viewed by 203

Editor


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Guest Editor
Department of Pathology, Yale University, New Haven, CT 06520, USA
Interests: cancer biology; urologic cancer

Special Issue Information

Dear Colleagues,

Over 80,000 new patients are diagnosed with bladder cancer each year in the United States. Despite the advancement of surgical techniques and the development of immunotherapy, the long-term prognosis of this disease remains poor, mainly due to genome and phenotypic diversity.

Currently, the paradigm shift in therapy for bladder cancer is transitioning from one-size-fits-all to personalized medicine based on the molecular subtypes' classification, mainly including luminal and basal subtypes. This subtype signature leads to the distinction of tumor progression and metastasis and further affects the susceptibility to traditional chemotherapy and targeted drugs.

This Special Issue of the International Journal of Molecular Sciences (IJMS) invites you to submit research articles elucidating the molecular mechanisms of bladder cancer progression and review in this field. Particularly, we encourage you to submit research articles focusing on the distinction across molecular subtypes of bladder cancer.

Additionally, the topics including tumor microenvironment, epigenetic regulation, and biomarkers are also welcome to enhance our comprehensive understandings of this disorder.

I look forward to receiving your contributions.

Dr. Hironobu Yamashita
Guest Editor

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Keywords

  • urothelial carcinoma
  • molecular subtypes
  • tumor microenvironment (TME)
  • epigenetics
  • precision medicine
  • chemoresistance

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Published Papers (1 paper)

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Review

33 pages, 1350 KB  
Review
Matricellular Proteins in Bladder Cancer: Context-Dependent Roles in Tumor Promotion and Suppression
by Azamat Akhmetkaliyev, José Héctor Gibrán Fritz García, Eva Sonnenberg-Riethmacher and Dieter Riethmacher
Int. J. Mol. Sci. 2026, 27(15), 6807; https://doi.org/10.3390/ijms27156807 - 29 Jul 2026
Abstract
Bladder cancer (BLCA) is a common and heterogeneous malignancy in which disease progression is driven not only by tumor-intrinsic alterations but also by dynamic interactions within the tumor microenvironment (TME). Increasing evidence positions the extracellular matrix (ECM) as a critical regulator of these [...] Read more.
Bladder cancer (BLCA) is a common and heterogeneous malignancy in which disease progression is driven not only by tumor-intrinsic alterations but also by dynamic interactions within the tumor microenvironment (TME). Increasing evidence positions the extracellular matrix (ECM) as a critical regulator of these processes. Matricellular proteins (MCPs), a group of nonstructural ECM-associated molecules, have emerged as key modulators of tumor–stroma communication. In BLCA, MCPs have been reported to display divergent, and in some cases opposing, associations or functions, with the same protein participating in both tumor promotion and suppression. Here, we review current evidence on the function of MCPs in BLCA and synthesize their bidirectional roles in carcinogenesis. MCPs contribute to tumor progression by promoting invasion, epithelial–mesenchymal transition (EMT), angiogenesis, and metastatic niche formation. At the same time, MCPs can restrain tumor growth by inhibiting angiogenesis, stabilizing ECM organization, inducing cell cycle arrest, and maintaining epithelial integrity. A key concept emerging from this body of evidence is the context-dependent functional plasticity of MCPs. We propose that MCP-associated phenotypes in BLCA may be influenced by contextual factors, including isoform diversity arising from alternative splicing and post-translational modifications, spatial compartmentalization within tumor and stromal niches, tumor microenvironmental composition, and molecular subtype. However, the level of supporting evidence differs substantially among MCPs, and direct BLCA-specific mechanistic evidence remains limited for many proposed relationships. These factors, therefore, provide a framework for interpreting divergent findings rather than representing universally established determinants of MCP function. Recognizing MCPs as context-sensitive regulators rather than fixed tumor-promoting or tumor-suppressing entities provides a unifying framework for understanding their roles in BLCA. This could be an important step for therapeutic targeting, encouraging effective strategies to consider and incorporate the molecular and microenvironmental context in which MCPs operate. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Bladder Cancer)
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