Circular RNAs (circRNAs) are a class of endogenous non-coding RNAs characterized by covalently closed loop structures, which confer high stability and evolutionary conservation. Beyond their well-known role as microRNA sponges, circRNAs can directly interact with proteins to modulate protein stability, activity, subcellular localization, and transcriptional or epigenetic regulation. These circRNA–protein interactions play critical roles in cancer progression by influencing tumor cell proliferation, metastasis, stemness, metabolic reprogramming, cell death, and therapy resistance. Moreover, they can shape the tumor immune microenvironment, affecting immune cell infiltration, immune evasion, and responses to immunotherapy. Understanding the mechanisms and functional consequences of circRNA–protein interactions provides new insights into tumor biology and offers promising avenues for cancer diagnosis, prognosis, and therapeutic intervention.

N-acetyltransferase 10 (NAT10), the primary writer of N4-acetylcytidine (ac4C) on RNA, is broadly upregulated across multiple cancer types and correlates with tumor proliferation, invasion, therapeutic resistance, and poor prognosis, indicating its significant clinical relevance. In this mini review, we systematically summarize the functional roles and mechanisms of NAT10-mediated ac4C modification in both normal development and cancer. Specifically, we cover recent advances in the regulation of mRNA stability and translation, as well as modifications of tRNA, long non-coding RNA (lncRNA), microRNA (miRNA), and circular RNA (circRNA). Moreover, we integrate evidence supporting the essential roles of NAT10 in embryonic development, gametogenesis, stem cell self-renewal and differentiation, cellular architecture and cell cycle control, and immune cell expansion, while outlining its oncogenic contributions to tumor growth, metastasis, metabolic reprogramming, drug resistance, and immune evasion. Based on clinical findings, we discuss the potential of NAT10 as a diagnostic and prognostic biomarker and its application in liquid biopsy, and we evaluate the therapeutic potential and limitations of targeting NAT10, including toxicity, specificity, and resistance. Finally, we propose future research directions, including the tumor-specific mechanisms driving NAT10 upregulation, strategies for selectively targeting cancer versus normal physiology, identification of ac4C readers and erasers, and potential crosstalk between ac4C and chromatin modification, with the aim of advancing NAT10-based precision oncology.

Objective To clarify the clinical significance and biological function of retinol dehydrogenase-11 (RDH11) in prostate cancer (PCa) and to elucidate the downstream signaling mechanism through which it drives tumor progression.Methods Public and in-house transcriptomic data were mined to compare RDH11 levels between PCa and matched normal tissues. RDH11 was stably silenced (shRDH11) or over-expressed (oeRDH11) in PC-3, DU145, and LNCaP cells; cell proliferation, migration, and invasion were quantified with CCK-8 and Transwell assays. RNA-seq and gene set enrichment analysis (GSEA) were performed to screen downstream targets and pathways. Rescue experiments in vitro and in vivo were used to confirm the mechanism.Results RDH11 levels were markedly elevated in human PCa tissues and cell lines. Silencing RDH11 hindered PCa cell proliferation, migration, and invasion, whereas its overexpression had the opposite effects. Mechanistically, we identified the tropomyosin receptor kinase (TRKA) and STAT3 signaling pathway as the downstream gene and pathway of RDH11. Rescue assays using PC3, DU145, and LNCaP cells demonstrated that RDH11 facilitated PCa progression by upregulation of TRKA and the activation of STAT3 signaling. In vivo studies further confirmed that RDH11 overexpression enhanced prostate tumor growth, whereas TRKA knockdown counteracted the oncogenic effects of RDH11.Conclusion RDH11 promotes the development of PCa through the upregulation of TRKA and activation of the STAT3 signaling pathway.

Myeloid sarcoma (MS) can manifest as a primary disease entity, known as de novo myeloid sarcoma, without the concurrent presence of acute or chronic myelocytic leukemia, myelodysplastic syndrome, or myeloproliferative neoplasm. It is crucial to approach suspected de novo myeloid sarcoma cases comprehensively to prevent misdiagnosis and ensure timely and accurate treatment. We report a case of de novo myeloid sarcoma involving the kidney in a 38-year-old female patient with a chief complaint of a rapidly enlarging palpable mass in the upper right quadrant for over a month. The patient's enhanced abdominal CT scan result was initially suspected to be renal cell carcinoma. Subsequently, we performed radical nephrectomy and post-operative pathology, immunohistochemistry, and cytogenetic analysis to confirm the diagnosis of de novo myeloid sarcoma. Histopathological analysis confirmed malignancy originating from the right kidney, accompanied by necrosis. The tumor cells displayed moderate size, evident pleomorphism, and off-centered granular cytoplasm. Extensive infiltration of the renal parenchyma was observed, involving the renal capsule, perirenal adipose tissue, and renal pelvis mucosa. CD117 displayed positive immunohistochemical staining. There is currently a dearth of studies that comprehensively describe de novo myeloid sarcoma involving the urogenital tract. In light of this gap in the literature, the present study aims to provide a systematic literature review and present a case of de novo myeloid sarcoma involving the kidney in patients with normal bone marrow biopsy. Our objective is to elucidate the clinical presentation and prognosis of de novo myeloid sarcoma involving the urogenital tract, thereby contributing to the existing knowledge base, and facilitating evidence-based treatment decisions. The multifaceted nature of MS necessitates a multidisciplinary approach, including thorough diagnostic evaluation involving immunohistochemistry, cytochemistry, and cytogenetic analysis. Standardizing terminology and refining diagnostic and treatment algorithms through future prospective studies are vital steps toward enhancing clinical management and prognosis for patients with de novo myeloid sarcoma of the urogenital tract.

Background Traditional estimates can only provide static predictions of cancer outcomes and cannot assess the evolving effect of race on patient survival. This study aims to reveal the dynamic survival of patients with bladder cancer and to explore the evolving effect of race on patient prognosis. Methods Using data from the Surveillance, Epidemiology, and End Results (SEER) registry, 99,590 white, 6,036 African American, and 4,685 Asian/Pacific Islander (API) patients with bladder cancer were identified. Conditional cancer-specific survival (CSS) rates, which could reflect the dynamic survival prediction of cancer patients, represented the primary outcomes, and were estimated by the Kaplan-Meier algorithm. The evolving effect of race on patient survival was evaluated by multivariable Cox regression in combination with conditional survival (CS) estimates. Results The 5-year CSS for African American patients who had survived 1, 2, 3, 4, or 5 years after definitive therapy improved from the baseline calculation by + 5.8 (84.4%), + 9.5 (87.4%), + 12.8 (90.0%), + 14.4 (91.3%), and + 14.7% (91.5%), respectively. The increasing trend also held for overall white and API patients, and for all patient subsets when CS was calculated according to different levels of sex, age, and disease stage. African Americans, despite having the worst survival at baseline, could have CSS comparable to their white and API counterparts after 4 years of survivorship. In addition, the risk of death for African Americans tended to decrease with increasing survival, and the risk was no longer significantly different from that of whites after 4 years of survival. Conclusions While having the worst initial predicted outcomes, African Americans may eventually achieve comparable survival to white and API patients given several years of survivorship. As patient survival increases, African American race may lose its role as an indicator of poorer prognosis.

BACKGROUND:Regulator of chromosome condensation 2 (RCC2) was a telophase disk-binding protein on mitosis, and functions as an oncogene in many human cancers. However, its role on prostate cancer (PCa) was unknown. The goal of this study is to explore the function of RCC 2 on PCa development.METHODS:The expression of RCC2 and its methylation level, its correlation with lymph node metastasis or disease-free survival (DFS) was analyzed using TCGA database. The effect of RCC2 on PCa cell proliferation, migration and invasion were detected using CCK-8, cell colony formation, Transwell and wood healing assays. RNA-seq and GSEA analysis were used to search the downstream genes and pathways of RCC2 in mediated PCa progression. Western blot was used to detect the proteins in PCa cells transfected with indicated siRNAs or plasmids.RESULTS:RCC2 had high expression and low promoter methylation level in PCa, and its expression was correlated with regional node metastasis and disease-free survival. Cell proliferation, migration, invasion and EMT of PCa cells in vitro were greatly enhanced after RCC2 overexpression, while the RCC2 knockdown suppressed these processes. RNA-seq and GSEA results showed the Hedgehog signaling regulator Gli1 and Gli3 were involved in RCC2 knockdown DU145 cells. Gli1 was also a marker of cancer stem-like cells (CSCs). Mechanistically, RCC2 induced cell growth, EMT, CSCs markers through Gli1; inhibiting Gli1 expression using siGli1 or GLI inhibitor suppressed cell progression in vitro and tumor growth in vivo.CONCLUSION:In summary, RCC2 promoted PCa development through Hh/Gli1 signaling pathway via regulating EMT and CSCs.

The application of Cu2+/peroxymonosulfate (PMS) process for the elimination of refractory pollutants in industrial wastewater is limited by the slow transformation from Cu2+ to Cu+. In this research, hydroxylamine (HA) was employed to improve the degradation capacity of the Cu2+/PMS process. Rhodamine B (RhB) was selected as the target compound to indicate the performance of HA/Cu2+/PMS process. Compared with the Cu2+/PMS process, the reduction of Cu2+ to Cu+ was effectively promoted by HA in the HA/Cu2+/PMS process, which increased the decomposition rate of PMS by 29.2

Background: Prostate cancer (PCa) is the second most common cancer among men worldwide. Perineural invasion (PNI) was a prominent characteristic of PCa, which was recognized as a key factor in promoting PCa progression. As a complex and heterogeneous disease, its true condition is difficult to explain thoroughly with conventional bulk RNA sequencing. Thus, an improved understanding of PNI-PCa progression at the single-cell level is needed. Methods: In this study, we performed scRNAseq on tumor tissues of three PNI-PCa patients. Principal component analysis (PCA) and Uniform manifold approximation and projection (UMAP) were used to reduce dimensionality and visualize the cellular composition of tumor tissues. The differently expressed genes among each cluster were identified by EdgeR. GO enrichment analysis was used to understand the roles of genes within the clusters. Pseudotime cell trajectory was used to reveal the molecular pathways underlying cell fate decisions and identify genes whose expression changed as the cells underwent transition. We applied CellPhoneDB to identify cell-cell interactions among the epithelial and neural cells in PNI-PCa. Results: Analysis of the ∼17,000 single-cell transcriptomes in three PNI prostate cancer tissues, we identified 12 major cell clusters, including neural cells and two epithelial subtypes with different expression profiles. We found that basal/intermediate epithelial cell subtypes highly expressed PCa progression-related genes, including PIGR, MMP7, and AGR2. Pseudotime trajectory analysis showed that luminal epithelial cells could be the initiating cells and transition to based/intermediate cells. Gene ontology (GO) enrichment analysis showed that pathways related to cancer progressions, such as lipid catabolic and fatty acid metabolic processes, were significantly enriched in basal/intermediate cells. Our analysis also suggested that basal/intermediate cells communicate closely with neural cells played a potential role in PNI-PCa progression. Conclusion: These results provide our understanding of PNI-PCa cellular heterogeneity and characterize the potential role of basal/intermediate cells in the PNI-PCa progression.

为了探究并优化钴离子(Co2+)活化过一硫酸盐(PMS)对水中抗生素的去除能力,以典型抗生素磺胺甲恶唑(SMX)为目标物,研究了反应体系对SMX的降解情况.考察了 Co2+投量、SMX浓度、PMS投量、温度和pH等因素对SMX降解效能的影响,并对反应体系的总有机碳(TOC)和活性物种进行分析.结果表明,常温条件下,Co2+浓度为0.05 mmol·L-1,PMS浓度为0.1 mmaol·L-1,SMX浓度为0.01 mmol·L-1,pH为3.0时降解效果最佳,当反应时间为30 min时,SMX降解率为62.3％,TOC去除率为47.7％.自由基淬灭分析表明,硫酸根自由基(SO4-·)是Co2+/PMS体系降解SMX的主导自由基.

为了防止石墨的氧化,在不添加任何粘结剂的情况下,通过激光烧结金属铝和二氧化硅粉,在石墨基片上原位制备出莫来石抗氧化涂层.对莫来石和SiO2涂层的相组成、显微组织、Vickers硬度和抗氧化性能进行了研究.结果表明:涂层中主要生成了莫来石及少量氧化铝和二氧化硅;在石墨表面形成致密且无裂纹的莫来石涂层;柱状莫来石晶体镶嵌在氧化硅玻璃相中,增强了涂层与基体之间的粘附性;莫来石涂层的Vickers硬度达到910 HV0.5.该涂层材料在长时间高温下显示出优异的抗氧化性能.激光烧结合成莫来石的主要反应机理为铝和二氧化硅的液相反应.