Migrasomes are a newly discovered type of extracellular vesicle (EV) formed during cell migration, playing a pivotal role in intercellular communication. These vesicles are generated by retracting fibers of migrating cells and encapsulate various molecules, such as proteins, lipids, and RNA, allowing the transfer of biochemical signals to neighboring cells. Current evidence suggests that migrasomes are involved in a wide range of physiological processes such as embryogenesis, angiogenesis, immune modulation, and mitochondrial quality control. Moreover, migrasomes are implicated in pathological conditions, including cancer metastasis, cardiovascular diseases, and viral infections. To fully understand their significance, it is critical to first explore the molecular mechanisms underlying their formation and function. Recent studies have shed light on the biogenesis, release, and biological properties of migrasomes, all of which are key to understanding their role in cell-to-cell communication. In this review, we provide an up-to-date summary of migrasome biogenesis, release, characterization, and their biological activities in intercellular communication, while also proposing potential new functions for these vesicles.

Background. Bladder cancer (BLCA) is a highly malignant tumor that develops in the urinary system. Identification of biomarkers in progression and prognosis is crucial for the treatment of BLCA. BLCA-related differentially expressed genes (DEGs) were authenticated by screening the DEGs and weighted gene coexpression network analysis (WGCNA). LASSO and SVM-RFE algorithms were utilized to screen the feature genes in BLCA. Survival analysis was performed using the KaplanMeier curve provided by the survival R package. The BLCA samples were clustered by hclust based on the immune score matrix calculated by the single-sample GSEA (ssGSEA) algorithm. The immune, stromal, and ESTIMATE scores of each BLCA patient were calculated by applying the ESTIMATE algorithm. ssGSEA was conducted to explore the function of characteristic genes in BLCA. The expression of characteristic genes in clinical cancer tissue, and the pericancerous tissue of BLCA patients was verified using qRT-PCR assays. A total of 189 BLCA-related DEGs were identified. Fourteen feature genes were defined by LASSO and SVM-RFE algorithms. Five characteristic genes, including SMYD2, GAPDHP1, ATP1A2, CILP, and THSD4, were related to the OS of BLCA. The correlation analysis of five characteristic genes and clinicopathological factors showed that five genes played a role in the progression of BLCA. Additionally, the expression of five characteristic genes in clinical cancer tissues and pericarcinomatous tissues from BLCA patients was verified by qRT-PCR, which was consistent with the result from the public database. Finally, we discovered five prognostic genes linked to BLCA progression, which might serve as a theoretical basis for prognosis and treatment targets for BLCA patients.

Bladder cancer (BC) is a prevalent urinary malignancy characterized by high recurrence rates and suboptimal long-term outcomes from traditional treatments such as surgery, chemotherapy, and radiotherapy. T-cell-based immunotherapy has emerged as a promising approach, harnessing T cells’ capacity to target and destroy tumor cells, yet it faces challenges from the immunosuppressive tumor microenvironment (TME), immune evasion, and T-cell exhaustion. Nanomaterials offer innovative solutions by enabling targeted delivery of antigens, checkpoint inhibitors, and immunomodulators; remodeling the TME through metabolic interventions (eg, hypoxia alleviation and adenosine reduction); and enhancing T-cell infiltration and persistence with stimulus-responsive systems like pH-sensitive nanoparticles and biomimetic vesicles. This review systematically examines nanomaterial integration to amplify T-cell-mediated immunity in BC, covering T-cell origins, differentiation (eg, CD8+ cytotoxic and CD4+ helper subsets), roles in the TME, and exhaustion mechanisms driven by factors like PD-1 and TOX. We discuss key strategies including direct immune enhancement via immunogenic cell death induction, metabolic reprogramming to optimize T-cell function, and sustained activation for improved persistence. In conclusion, these nanomaterial-enhanced therapies address critical barriers, promoting precise and synergistic immune responses. Future prospects highlight AI-driven designs, personalized medicine, and clinical translation to tackle heterogeneity, biosafety, and resistance for durable BC remission.

The metabolism of arginine, a conditionally essential amino acid, plays a crucial role in cancer progression and prognosis. However, a more detailed understanding of the influence of arginine biosynthesis genes in cancer is currently unavailable. We performed an integrative multi-omics analysis using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to determine the characteristics of these genes across multiple cancer types. To measure the overall activity of arginine biosynthesis genes in cancer, we calculated arginine biosynthesis scores based on gene expression. Our results indicated that the arginine biosynthesis score was negatively correlated with immune-related pathways, immune infiltration, immune checkpoint expression, and patient prognosis, and single-cell data further clarified that patients with high arginine biosynthesis scores showed a reduced proportion of T and B cells in an immune desert tumor microenvironment and were insensitive to immunotherapy. We also identified several potential drugs through the Cancer Therapeutic Response Portal (CTRP) and Genomics of Drug Sensitivity in Cancer (GDSC) databases that could target arginine biosynthesis genes and potentially improve the response rate to immunotherapy in patients with a high arginine biosynthesis fraction. Overall, our analyses emphasize that arginine biosynthesis genes are associated with immune evasion in several cancers. Targeting these genes may facilitate more effective immunotherapy.

The global incidence of prostate cancer (PCa) is rising. Localized PCa can be managed through surgical intervention or radiotherapy, but certain patients may experience recurrence or develop metastatic disease following localized treatment. Despite aggressive therapeutic approaches, the majority of metastatic patients with PCa will eventually progress to metastatic castration‑resistant PCa, with limited treatment alternatives and a dismal prognosis. The treatment options for advanced PCa are continuously evolving, yet there remains a demand for further innovative therapeutic approaches. Antibody‑drug conjugates (ADCs) represent a novel class of targeted medications comprising a humanized monoclonal antibody, a linker and a cytotoxic payload. ADCs primarily bind to antigens that are upregulated on the surface of PCa cells but are minimally expressed on normal cells. At present, a variety of targets for ADCs have been identified in the treatment of PCa, encompassing prostate‑specific membrane antigen, STEAP family member 1, trophoblast cell‑surface antigen 2, CD46, B7‑H3, tissue factor and delta‑like protein 3, each with one or more specific ADC that has shown encouraging results in the PCa field. In the present review, the developmental course, composition and mechanism of action of ADCs are explored, with a specific focus on recently published studies and ongoing trials aimed at investigating the efficacy and safety of ADCs in treating PCa. Lastly, ongoing challenges in ADC development and corresponding strategies to combat them are discussed.

Bladder cancer (BLCA) is a prevalent malignancy with substantial consequences for patient health. This study aimed to elucidate the underlying mechanisms of BLCA through integrated multi-omics analysis. Tumor and adjacent tissues from BLCA patients underwent transcriptomic, whole-exome sequencing, metabolomic, and intratumoral microbiome analyses. These data were integrated with public datasets to identify key genes, metabolites, and microorganisms. Molecular subtypes were defined by key gene expression and compared for pathways, immune profiles, mutations, immunotherapy response, and drug sensitivity. Prognostic relevance was validated in external cohorts. Single-cell sequencing was applied to reveal cellular localization of key genes. Three key genes (AHNAK, CSPG4, NCAM1), 90 metabolites, and two microbes (Sphingomonas koreensis, Rhodospirillaceae) were identified. Key genes negatively correlated with metabolites but not with microbes. BLCA samples were classified into two molecular clusters with distinct ECM organization, metabolic features, immune checkpoint expression, and therapeutic sensitivity. NCAM1 correlated positively with γδ T cells and negatively with M0 macrophages. Single-cell analysis revealed nine major cell types, with fibroblasts displaying the highest expression of key genes, particularly elevated AHNAK in specific fibroblast subtypes. Drug prediction and docking identified candidate compounds targeting these genes with stable binding potential. This comprehensive multi-omics analysis links key genes, metabolites, and microbes to BLCA pathogenesis. Fibroblasts emerge as central regulators, while identified gene-metabolite interactions and microbial associations provide novel insights into tumor heterogeneity. These findings highlight potential biomarkers and therapeutic targets to support precision treatment in BLCA.