The exosome is a critical component of the intercellular communication., playing a vital role in regulating cell function. These small vesicles contain proteins, mRNAs, miRNAs, and lncRNAs, surrounded by lipid bilayer substances. Most cells in the human body can produce exosomes, released into various body fluids such as urine, blood, and cerebrospinal fluid. Bladder cancer is the most common tumor in the urinary system, with high recurrence and metastasis rates. Early diagnosis and treatment are crucial for improving patient outcomes. This study employed the PubMed search engine to retrieve publicly accessible data pertaining to urinary exosomes. We summarize the origins and intricate biological characteristics of urinary exosomes, the introduction of research methodologies used in basic experiments to isolate and analyze these exosomes, the discussion of their applications and progress in the diagnosis and treatment of bladder cancer, and the exploration of the current limitations associated with using urinary exosomes as molecular biomarkers for diagnosing bladder cancer. Exosomes isolated from urine may be used as molecular biomarkers for early detection of bladder cancer.

N-acetyltransferase 10 (NAT10), an enzyme responsible for ac4C acetylation, is implicated in cancer progression, though its specific biological function in prostate cancer remains insufficiently understood. This study clarifies NAT10’s role in prostate cancer and its effects on the tumor immune microenvironment. NAT10 expression and clinical relevance were assessed through bioinformatics, RT-qPCR, and IHC analyses, comparing prostate cancer tissues with normal controls. The impact of NAT10 on tumor cell proliferation, migration, and invasion was investigated via in vitro assays—including CCK-8, EdU, wound healing, and 3D-Transwell—as well as in vivo mouse xenograft models and organoid studies. Further, NAT10’s influence on immune cell infiltration was examined using flow cytometry, IHC, cell co-culture assays, and ELISA to elucidate downstream chemokine effects, specifically targeting CD8⁺ T cells. Findings indicated significant upregulation of NAT10 in prostate cancer cells, enhancing their proliferative and invasive capacities. Notably, NAT10 suppresses CD8⁺ T cell recruitment and cytotoxicity through the CCL25/CCR9 axis, fostering an immunosuppressive microenvironment that exacerbates tumor progression. An ac4C modification score was also devised based on NAT10’s downstream targets, providing a novel predictive tool for evaluating immune infiltration and forecasting immunotherapy responses in patients with prostate cancer. This study underscores NAT10’s pivotal role in modulating the prostate cancer immune microenvironment, offering insights into the immune desert phenomenon and identifying NAT10 as a promising therapeutic target for improving immunotherapy efficacy.

Objective: The prognosis of patients with prostate cancer (PCa) has improved in recent years, but treatment-related cardiotoxicity remains unclear. This study investigated the heart-specific mortality and prognostic factors of patients with PCa after radiotherapy (RT) or radical prostatectomy (RP), and compared their long-term heart-specific mortality with that of the general male population.Materials and Methods: Data were taken from the Surveillance, Epidemiology, and End Result (SEER) database. Patients with PCa were included who underwent RT or RP from 2000 to 2012, and were followed through 2015. A cumulative mortality curve and a competitive risk regression model were applied to assess the prognostic factors of heart-specific mortality. Standardized mortality rates (SMRs) were calculated.Results: Of 389,962 men, 49.7% and 50.3% received RP and RT, respectively. The median follow-up was 8.3 years. For patients given RT, in about 9 years postdiagnosis, the cumulative mortality due to heart-specific disease exceeded that due to PCa. In patients who underwent RP, cumulative mortality from heart-specific disease or PCa was comparable. Relative to the general male population, overall, the heart-specific mortality of patients with PCa receiving RT or RP was not higher, but in patients aged 70 to 79 years, those given RT experienced slightly higher heart-specific mortality than the age-matched general population.Conclusions: Patients with PCa treated with RT or RP overall do not incur risk of heart-specific mortality higher than that of the general male population, except for patients aged 70–74 years receiving RT.

Prostate cancer (PCa) metastasis has emerged as a leading cause of mortality globally. Owing to the distinctive looping structure, circular RNA has become an ideal biological tumor marker. Here we investigate the mechanism and function of circular RNA, specifically circCNOT6L, on PCa metastasis. A loss-of-function assay was conducted in vitro to assess the impact of circCNOT6L on cancer cell proliferation, migration, invasion and ferroptosis. In addition, a xenograft mouse model was used to elucidate the influence of circCNOT6L on subcutaneous tumor xenograft and lung metastasis. Biochemical experiments elucidated the molecular mechanism by which circCNOT6L promotes malignant progression in PCa cells by modulating ferroptosis. Moreover, the combination of circCNOT6L-si and a ferroptosis activator was tested in organoids to evaluate their potential as suppressors of tumorigenesis. The novel circular RNA, circCNOT6L, was highly expressed in both PCa metastatic tissues and cells. circCNOT6L suppression resulted in a notable inhibition in PCa cell migration, invasion and ferroptosis in vitro. Furthermore, circCNOT6L inhibition hindered the growth and metastasis of mouse xenografts. Mechanistically, circCNOT6L, generated by the RNA-binding protein EIF4A3, competes with miR-143-5p for binding, thereby facilitating SRSF2-dependent splicing of SLC7A11 precursor RNA. This process inhibited ferroptosis in PCa cells and promoted PCa progression. Finally, inhibiting circCNOT6L overexpression in combination with the ferroptosis activator (erastin) significantly suppressed the viability of PCa-derived organoids. In conclusion, in the present study, we found that circCNOT6L induced by EIF4A3 through the SRSF2–SLC7A11 axis effectively inhibits ferroptosis, which in turn promotes malignant progression of PCa.

Circular RNAs (circRNAs) play crucial biological functions in various tumors, including bladder cancer (BCa). However, the roles and underlying molecular mechanisms of circRNAs in the malignant proliferation of BCa are yet unknown. CircKDM1A was observed to be downregulated in BCa tissues and cells. Knockdown of circKDM1A promoted the proliferation of BCa cells and bladder xenograft growth, while the overexpression of circKDM1A exerts the opposite effect. The dual-luciferase reporter assay revealed that circKDM1A was directly bound to miR-889-3p, acting as its molecular sponge to downregulate CPEB3. In turn, the CPEB3 was bound to the CPE signal in p53 mRNA 3′UTR to stabilize its expression. Thus, circKDM1A-mediated CPEB3 downregulation inhibits the stability of p53 mRNA and promotes BCa malignant progression. In conclusion, circKDM1A functions as a tumor suppressor in the malignant proliferation of BCa via the miR-889-3p/CPEB3/p53 axis. CircKDM1A may be a potential prognostic biomarker and therapeutic target of BCa.