Explore the vast range of titles available.

The digital economy (DE) has become a major breakthrough in promoting industrial upgrading and an important engine for high-quality economic growth. However, most studies have neglected the important driving effect of regional economic and social (RES) development on DE. In this paper, we discuss the mechanism of RES development promoting the development of DE, and establish a demand-driven regional DE development model to express the general idea. With the help of spatial analysis toolbox in ArcGIS software, the spatial development characteristics of DE in the Yangtze River Delta City Cluster (YRDCC) is explored. We find the imbalance of spatial development is very significant in YRDCC, no matter at the provincial level or city level. Quantitative analysis reveals that less than 1% likelihood that the imbalanced or clustered pattern of DE development in YRDCC could be the result of random chance. Geographically weighted regression (GWR) analysis with publicly available dataset of YRDCC indicates RES development significantly promotes the development of DE.

Information consumption is a kind of economic activity that directly or indirectly takes information products and information services as consumption objects. Most of the existing studies have established the \"formula” of rural information consumption in promoting economic and social development, while few efforts have been devoted to study the quantitative reciprocities between them. Therefore, this study aims to investigate the relationship between information consumption in rural areas and regional economic development with a case study of Zhejiang, China. Based on rural information consumption-related indexes, basic geographic data, and other publicly available regional economic development related data, we conduct the exploration with the spatial Durbin model (SDM). The study indicates that (1) from the perspective of spatial analysis, the economic development level of all prefecture-level cities in Zhejiang, China has a significant positive spatial correlation; (2) in rural areas, the network infrastructure improvement, information industry clustering, etc. can accelerate enhancing information consumption and promote regional economic development; and (3) facilitate the development of rural information consumption is conducive to alleviate the imbalance of regional economic development. It is hoped that our study can help understand the current situation of information consumption in rural China and provide a theoretical reference for rural economic and social development.

This study explored the spatio-temporal dynamics and evolution of land use/cover changes and urban expansion in Shanghai metropolitan area, China, during the transitional economy period (1979–2009) using multi-temporal satellite images and geographic information systems (GIS). A maximum likelihood supervised classification algorithm was employed to extract information from four landsat images, with the post-classification change detection technique and GIS-based spatial analysis methods used to detect land-use and land-cover (LULC) changes. The overall Kappa indices of land use/cover change maps ranged from 0.79 to 0.89. Results indicated that urbanization has accelerated at an unprecedented scale and rate during the study period, leading to a considerable reduction in the area of farmland and green land. Findings further revealed that water bodies and bare land increased, obviously due to large-scale coastal development after 2000. The direction of urban expansion was along a north-south axis from 1979 to 2000, but after 2000 this growth changed to spread from both the existing urban area and along transport routes in all directions. Urban expansion and subsequent LULC changes in Shanghai have largely been driven by policy reform, population growth, and economic development. Rapid urban expansion through clearing of vegetation has led to a wide range of eco-environmental degradation.

Bladder cancer (BC) is a malignant tumor characterized by a high incidence of urinary system diseases. The complex pathogenesis of BC has long been a focal point in medical research. With the robust development of epigenetics, the crucial role of epigenetic modifications in the occurrence and progression of BC has been elucidated. These modifications not only affect gene expression but also impact critical biological behaviors of tumor cells, including proliferation, differentiation, apoptosis, invasion, and metastasis. Notably, DNA methylation, an important epigenetic regulatory mechanism, often manifests as global hypomethylation or hypermethylation of specific gene promoter regions in BC. Alterations in this methylation pattern can lead to increased genomic instability, which profoundly influences the expression of proto-oncogenes and tumor suppressor genes. MiRNAs, as noncoding small RNAs, participate in various biological processes of BC by regulating target genes. Consequently, this work aims to explore the interaction mechanisms between DNA methylation and miRNAs in the occurrence and development of BC. Research has demonstrated that DNA methylation not only directly influences the expression of miRNA genes but also indirectly affects the maturation and functionality of miRNAs by modulating the methylation status of miRNA promoter regions. Simultaneously, miRNAs can regulate DNA methylation levels by targeting key enzymes such as DNA methyltransferases (DNMTs), thereby establishing a complex feedback regulatory network. A deeper understanding of the crosstalk mechanisms between DNA methylation and miRNAs in BC will contribute to elucidating the complexity and dynamics of epigenetic modifications in this disease, and may provide new molecular targets and strategies for the early diagnosis, treatment, and prognostic evaluation of BC.

CircRNAs are an important class of non-coding RNAs, which are produced via back-splicing of exons and/or intron sequences of precursor mRNAs and generally cannot be translated into proteins as they do not bind to ribosomes. There is varying evidence supporting the claim that circRNAs are abnormally expressed in cancer and play a crucial role in cancer initiation and progression. Ubiquitin is a highly stable protein that can be conjugated to target proteins. The most crucial role of ubiquitination is to mediate the degradation of substrate proteins by the proteasome. An increasing amount of evidence indicates that circRNAs are involved in the precise degradation of proteins via the ubiquitin-proteasome system. This review systematically summarizes the intricate mechanisms by which circRNAs regulate target protein ubiquitination, modulate cancerous signaling pathways, and control tumorigenesis and tumor development. Although studies are continuously uncovering additional complex interactions between circRNAs and proteins, we believe that circRNAs are promising but challenging molecules that have the potential to facilitate precise cancer therapies in the future.

The ubiquitin (Ub) system has been demonstrated to play a crucial role in various cellular processes, including immune responses, cell development, and programmed cell death. Ubiquitination, a form of post-translational modification, occurs in eukaryotic cells and involves several key components, such as Ub-activating enzymes, Ub-binding enzymes, and Ub-protein ligases. Recently, deubiquitinating enzymes—proteases that reverse the modification of proteins by removing Ub or Ub-like molecules, or by remodeling Ub chains on target proteins—have been identified as significant regulators of ubiquitination-mediated degradation. These enzymes profoundly influence cellular pathways and numerous biological processes, including the DNA damage response and DNA repair mechanisms. Recent studies increasingly demonstrate a relationship between ubiquitination, deubiquitination, and urinary diseases. The roles of these processes in urinary diseases are complex, encompassing various aspects of signaling, protein stability, and cellular metabolism. As research advances, the specific mechanisms by which these processes influence urologic diseases will be further clarified. This review examines recent discoveries in this field, aiming to provide new strategies and targets for the diagnosis and treatment of urologic diseases.

Tumors of the urinary system primarily encompass prostate, bladder, and kidney cancers, which exhibit high morbidity and mortality rates worldwide and pose a particularly significant threat to men’s health. Given the associated high morbidity and mortality, early diagnosis and effective treatment are crucial. Consequently, innovative research is urgently needed to enhance the clinical care of patients with urologic cancers. Recent studies have demonstrated that microRNAs (miRNAs), as key non-coding RNA molecules that regulate gene expression, play a vital regulatory role in malignant tumor development by binding to the mRNA 3′-UTR region. Large-scale genomic analyses (e.g., TCGA Pan-Cancer Atlas) reveal that over 50% of miRNA genes reside in cancer-associated regions, regulating >60% of protein-coding genes. miR-145 exemplifies this paradigm, with its dysregulation causally linked to tumor proliferation, metastasis, and therapy resistance. Among them, miR-145, as a regulatory molecule with significant anticancer properties, presents unique expression characteristics and functional mechanisms in urological tumours. In this review, we summarize the role of miR-145 in specific urological tumors, along with its downstream target molecules and cells, which may enhance our understanding of miR-145 in these cancers. In conclusion, miR-145 is a multifaceted regulator in urological oncology that has strong potential to range from non-invasive biomarker discovery to therapeutic strategies that work synergistically with conventional treatments, ultimately advancing precision medicine in prostate, bladder, and kidney cancers.

Kidney stones are a globally prevalent urological disease, with calcium oxalate stones being the most common type. Their pathogenesis is complex, and postoperative recurrence rates are high. The calcium-sensing receptor (CaSR) and solute carrier family 26 member 6 (SLC26A6) play key roles in hypercalciuria and hyperoxaluria, respectively. However, the intrinsic relationship and regulatory mechanism between them in kidney stone formation remain unclear. This study aims to investigate whether CaSR regulates SLC26A6 expression through a specific signaling pathway, thereby playing a role in experimental calcium oxalate kidney stone formation in rats. , a calcium oxalate kidney stone model was established in Wistar rats by intragastric administration of 1% ethylene glycol (E.G.,) and 1% ammonium chloride. Rats were divided into six groups: blank control (NC), E.G., model (E.G.,), CaSR agonist (CaSR-a), CaSR inhibitor (CaSR-i), protein kinase A inhibitor (PKA-i), and Forkhead box protein O4 inhibitor (FOXO4-i) groups. Urinary calcium and oxalate levels were measured. Kidney crystal formation was observed via Hematoxylin and Eosin (HE) staining and Pizzolato's staining. Protein and mRNA expression of CaSR, p-protein kinase A (PKA) substrate, p-FOXO4 (Thr451), and SLC26A6 in kidney tissues were detected by Western blotting, immunohistochemistry, and Real-Time quantitative PCR (RT-qPCR). , rat renal tubular epithelial cells (NRK-52E) were intervened with calcium oxalate monohydrate (COM) crystals and treated with agonists or inhibitors of CaSR, PKA, and Forkhead box protein O4 (FOXO4). Pathway-related protein expression was detected by Western blotting. A dual-luciferase reporter gene assay was used to validate the transcriptional regulation of the SLC26A6 promoter by FOXO4. Compared to the NC group, the, E.G., group showed significantly increased urinary calcium and oxalate concentrations, increased renal crystal deposition, and upregulated expression of CaSR, p-PKA substrate, p-FOXO4, and SLC26A6. Activating CaSR (CaSR-a group) further exacerbated these phenomena, whereas inhibiting CaSR (CaSR-i group), PKA (PKA-i group), or FOXO4 (FOXO4-i group) significantly alleviated crystal formation and reduced SLC26A6 expression. Cell experiments confirmed that activating CaSR enhanced PKA and FOXO4 phosphorylation and SLC26A6 expression; activating PKA enhanced FOXO4 phosphorylation and SLC26A6 expression; activating FOXO4 upregulated SLC26A6 expression. The dual-luciferase reporter gene assay showed that FOXO4 functionally regulates SLC26A6 promoter and regulates its transcriptional activity. During the formation of experimental calcium oxalate kidney stones in rats, CaSR activation promotes PKA-mediated FOXO4 phosphorylation, leading to upregulation of SLC26A6 expression through transcriptional mechanisms. This signaling axis promotes urinary oxalate excretion and contributes to kidney stone formation. This study reveals the potential role of the novel CaSR-PKA-FOXO4-SLC26A6 signaling pathway in the pathogenesis of kidney stones.

Hypoxia is a characteristic feature of the tumor microenvironment that significantly influences cancer progression and treatment responses. Hypoxia-inducible factor (HIF), a key regulator of hypoxic adaptation, has been demonstrated to modulate hypoxic gene expression profiles and signaling networks, thereby serving as a potential therapeutic target. Long-stranded non-coding RNAs (lncRNAs), defined as non-coding RNAs exceeding 200 nucleotides in length, regulate various cellular processes by modulating gene expression at transcriptional, post-transcriptional, and epigenetic levels. Evidence suggests that lncRNAs can be regulated by HIF at the transcriptional level. Conversely, HIF itself can be modulated by numerous lncRNAs, with alterations in these lncRNAs being associated with tumorigenesis, resulting in a reciprocal regulatory network. Recently, the critical role of lncRNAs in hypoxia-driven cancer progression has been elucidated in digestive tumors, including colorectal, pancreatic, gastric, and hepatocellular carcinomas. An increasing number of studies have revealed the complex interplay between lncRNAs and HIF in regulating various processes such as proliferation, metastasis, apoptosis, and drug resistance. In this paper, we aim to provide a comprehensive summary of recent advances regarding the roles of hypoxia and lncRNAs in digestive system tumors and to illustrate the mechanisms through which lncRNAs interact with hypoxia in tumor cells. This will enhance our understanding of the regulatory roles of lncRNAs in modulating the microenvironment of digestive system tumors, thereby facilitating the development of novel anticancer drugs.

[This corrects the article DOI: 10.3389/fcell.2025.1611889.].