Cell Cycle最新文献_第9页

Integration of a 4-gene risk score model enhances prognostic accuracy in acute myeloid leukemia. 整合4基因风险评分模型可提高急性髓性白血病的预后准确性。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-29 DOI: 10.1080/15384101.2025.2578389

Yiqing Li, Boqi Li, Jie Xiao, Kezhi Huang, Yuchan Liang, Peiting Zeng, Wenjuan Yang, Danian Nie

{"title":"Integration of a 4-gene risk score model enhances prognostic accuracy in acute myeloid leukemia.","authors":"Yiqing Li, Boqi Li, Jie Xiao, Kezhi Huang, Yuchan Liang, Peiting Zeng, Wenjuan Yang, Danian Nie","doi":"10.1080/15384101.2025.2578389","DOIUrl":"10.1080/15384101.2025.2578389","url":null,"abstract":"The clinical outcomes of acute myeloid leukemia (AML) patients exhibit substantial heterogeneity, with relapse posing a formidable challenge. Herein, we developed a risk score model by integrating relapse-related genes through Cox regression analysis. The relapse-related genes were identified via differential gene expression analysis of 15 matched diagnosed and relapsed AML samples retrieved from the Gene Expression Omnibus (GEO) database. These genes include SCN9A, CFH, CD34, and CALCRL. Our findings demonstrate that higher risk scores were significantly associated with an unfavorable ELN2017 risk classification, leukemic transformation, as well as FLT3-ITD and RUNX1 mutations. Conversely, lower risk scores were linked to NPM1 mutation. Patients with higher risk scores had a shorter overall survival (OS). Furthermore, we integrated the risk score model with the European LeukemiaNet (ELN) risk classification to establish a novel composite risk classification scheme. Patients were classified into three new risk groups based on composite risk classification showing significantly distinct OS. In summary, the four-gene risk score holds promise in predicting the OS of AML patients, and the composite risk classification shows greater potential in predicting the outcomes of AML patients. These four genes may represent potential therapeutic targets in the treatment of AML.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"638-654"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Influence of bacterial proteins on the host's cell cycle. 细菌蛋白对宿主细胞周期的影响。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-29 DOI: 10.1080/15384101.2025.2577757

Francesca Benedetti, Camila Summers, Robert C Gallo, Davide Zella

引用次数: 0

CKS2 promotes the malignant phenotypes of bladder cancer cells via PI3K/AKT signaling pathway activation. CKS2通过激活PI3K/AKT信号通路促进膀胱癌细胞的恶性表型。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-07 DOI: 10.1080/15384101.2025.2586117

Tao Yang, Shao-Peng Kong, Qing-Le Xu, Cheng-Xin Zhan, Xiao-Tong Wang, Shou-Bin Li, Gang Wang, Jian-Guo Ma

{"title":"CKS2 promotes the malignant phenotypes of bladder cancer cells via PI3K/AKT signaling pathway activation.","authors":"Tao Yang, Shao-Peng Kong, Qing-Le Xu, Cheng-Xin Zhan, Xiao-Tong Wang, Shou-Bin Li, Gang Wang, Jian-Guo Ma","doi":"10.1080/15384101.2025.2586117","DOIUrl":"10.1080/15384101.2025.2586117","url":null,"abstract":"Cyclin-dependent kinase subunit 2 (CKS2) has been implicated in various malignancies. This study investigates the mechanism by which CKS2 contributes to bladder cancer (BC) progression. Abnormally expressed genes were identified by differential analysis of tumor and normal tissues using Gene Expression Omnibus datasets. Subsequently, functional assays - including cell proliferation, Transwell migration, colony formation, wound healing, flow cytometry, and enzyme-linked immunosorbent assays - were performed to provide cellular evidence supporting the oncogenic function of CKS2 in BC. The results demonstrated significantly elevated CKS2 expression in BC cells than in normal urothelial cells. CKS2 overexpression promoted cell proliferation, cell migration and invasion. Mechanistically, CKS2 overexpression caused a marked reduction in PTEN protein levels, thereby inhibiting PIP3 degradation and indirectly activating the PI3K/AKT signaling pathway. Furthermore, CKS2 promoted phosphorylation and degradation of p27 Kip1 (Thr187), consequently contributing to cell cycle deregulation and further enhancing PI3K/AKT pathway activity. In contrast, CKS2 knockdown produced the opposite effects. Notably, treatment with the PI3K inhibitor LY294002 effectively reversed CKS2-induced BC cell proliferation and metastasis. In conclusion, CKS2 promoted the malignant phenotypes of BC cells by enhancing PI3K/AKT pathway activity through dual mechanisms involving PTEN downregulation and p27 Kip1-mediated cell cycle dysregulation.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"687-701"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma. lncRNA H19沉默抑制线粒体自噬：克服肺腺癌顺铂耐药的新策略

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-05 DOI: 10.1080/15384101.2025.2581634

Meng-Zhen Liu, Xiao-Yan Shao, Si-Han Wu, Qi-Qi Ning, Can Zhang, Wei-Wei Du, Rong-Rong Sun, San-Yuan Sun, You-Wei Zhang

{"title":"Mitophagy suppression via lncRNA H19 silencing: a novel strategy to overcome cisplatin resistance in lung adenocarcinoma.","authors":"Meng-Zhen Liu, Xiao-Yan Shao, Si-Han Wu, Qi-Qi Ning, Can Zhang, Wei-Wei Du, Rong-Rong Sun, San-Yuan Sun, You-Wei Zhang","doi":"10.1080/15384101.2025.2581634","DOIUrl":"10.1080/15384101.2025.2581634","url":null,"abstract":"Cisplatin (DDP) resistance substantially compromises treatment efficacy in lung adenocarcinoma (LUAD). This study investigates the role of mitochondrial long non-coding RNA (lncRNA) H19 in mediating DDP resistance. High-throughput sequencing and RT-qPCR analyses revealed pronounced H19 upregulation in DDP-resistant A549 (A549/DDP) cells relative to parental A549 cells. Subcellular localization studies indicated that H19 is primarily nuclear in A549 cells but translocates to mitochondria in A549/DDP cells. Functional assays demonstrated that H19 silencing in resistant cells attenuated chemoresistance, suppressed proliferation, migration, invasion, and colony formation in vitro, and delayed tumor growth in vivo. H19 knockdown impaired mitophagy and promoted apoptosis, mirroring autophagy inhibition and restoring DDP sensitivity. In contrast, H19 overexpression in A549 cells did not significantly alter mitophagy or cellular behavior. Furthermore, H19 silencing induced its relocalization from mitochondria back to the nucleus in resistant cells, while overexpression did not affect its nuclear localization. These findings establish that H19 translocation to mitochondria promotes DDP resistance, and its downregulation reverses this process by inhibiting mitophagy and resensitizing cells to DDP. As a nucleus-encoded mitochondria-associated lncRNA (ntmtlncRNA), H19 mediates intercompartmental communication, highlighting its potential as a therapeutic target for overcoming DDP resistance in LUAD.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"670-686"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptional cyclin-dependent kinases Cdk8 and Cdk19 are required for normal macrophage differentiation. 转录周期蛋白依赖性激酶Cdk8和Cdk19是正常巨噬细胞分化所必需的。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-22 DOI: 10.1080/15384101.2025.2571788

Aleksandra Kolodziejczyk, Samantha Liu, Fabian Strobel, Diego Martinez Alonso, Deborah Butter, Konrad Śnioch, Chen Chu, Henry Long, Veronika Sexl, Li Qiang, Stephanie K Dougan, Piotr Sicinski

{"title":"Transcriptional cyclin-dependent kinases Cdk8 and Cdk19 are required for normal macrophage differentiation.","authors":"Aleksandra Kolodziejczyk, Samantha Liu, Fabian Strobel, Diego Martinez Alonso, Deborah Butter, Konrad Śnioch, Chen Chu, Henry Long, Veronika Sexl, Li Qiang, Stephanie K Dougan, Piotr Sicinski","doi":"10.1080/15384101.2025.2571788","DOIUrl":"10.1080/15384101.2025.2571788","url":null,"abstract":"Cyclin-dependent kinases CDK8 and CDK19 together with their activating partner, cyclin C, regulate gene expression as a part of the Mediator complex and by phosphorylating DNA sequence-specific transcription factors. Here, we investigated the in vivo requirement for Cdk8 and Cdk19 in hematopoiesis by generating double knockout (DKO) mice lacking Cdk8 and Cdk19 expression in hematopoietic cells. DKO mice displayed relatively normal hematopoiesis and largely unperturbed gene expression in the bone marrow, indicating that the Mediator kinases are not essential for the regulation of gene expression during hematopoiesis. However, DKO mice showed an expansion of splenic macrophages. Bone marrow-derived DKO macrophages displayed an increased expression levels of both M1-like and M2-like markers, altered cytokine secretion, deregulated gene expression, precocious cell cycle exit and impaired Fc-mediated phagocytosis. Our findings reveal a highly cell type-specific role of Cdk8/19 in gene transcription during hematopoiesis.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"619-637"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Astrocyte-derived stanniocalcin-1 orchestrates epileptogenesis through NF-κB-dependent neuroinflammation. 星形胶质细胞衍生的斯坦钙素-1通过NF-κ b依赖性神经炎症协调癫痫发生。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-09-29 DOI: 10.1080/15384101.2025.2566293

Xinyue Guan, Wenzeng Wang, Qiannan Song, Kexin Li, Hong Chen

{"title":"Astrocyte-derived stanniocalcin-1 orchestrates epileptogenesis through NF-κB-dependent neuroinflammation.","authors":"Xinyue Guan, Wenzeng Wang, Qiannan Song, Kexin Li, Hong Chen","doi":"10.1080/15384101.2025.2566293","DOIUrl":"10.1080/15384101.2025.2566293","url":null,"abstract":"Background: This study aimed to investigate the expression pattern of astrocyte-derived STC1 in TLE and elucidate the molecular mechanisms by which STC1 regulates neuroinflammation and seizures through the NF-κB signaling pathway.Methods: A TLE model was established by intrahippocampal injection of kainic acid (KA) in mice. STC1 expression levels and cellular localization in the hippocampus of TLE mice were examined. Adeno-associated virus-mediated gene overexpression and shRNA knockdown approaches were employed to investigate the effects of STC1 on neuroinflammatory responses, neuronal survival, and seizure activity. qRT-PCR and immunofluorescence methods were further utilized to evaluate inflammatory cytokine levels and NF-κB signaling pathway activity.Results: STC1 expression was upregulated in hippocampal tissues of TLE mice, with double immunofluorescence showing STC1 predominantly localized in GFAP-positive reactive astrocytes. STC1 overexpression significantly exacerbated KA-induced neuroinflammation, along with enhanced microglial activation. STC1 knockdown attenuated neuroinflammatory responses. Nissl staining and NeuN immunohistochemistry confirmed that STC1 aggravated KA-induced neuronal loss. STC1 overexpression promoted p65 phosphorylation and nuclear translocation, activating the NF-κB signaling pathway.Conclusion: This study reveals the molecular mechanism by which astrocyte-derived STC1 promotes TLE-associated neuroinflammation and neuronal injury through activation of the NF-κB signaling pathway, elucidating the crucial role of the astrocyte-STC1-NF-κB axis in epileptogenesis.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"586-604"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The dual role of circular RNAs in paclitaxel resistance: insights into molecular mechanisms and clinical implications. 环状rna在紫杉醇耐药中的双重作用：分子机制和临床意义。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-17 DOI: 10.1080/15384101.2025.2575050

Ehsan Maghrebi-Ghojogh, Omer Qutaiba B Allela, Karar H Alfarttoosi, Sada Ghalib Taher, Mariem Alwan, Mahmood Jawad, Hiba Mushtaq, Mitra Zareanshahraki, Hossein Gandomkar

{"title":"The dual role of circular RNAs in paclitaxel resistance: insights into molecular mechanisms and clinical implications.","authors":"Ehsan Maghrebi-Ghojogh, Omer Qutaiba B Allela, Karar H Alfarttoosi, Sada Ghalib Taher, Mariem Alwan, Mahmood Jawad, Hiba Mushtaq, Mitra Zareanshahraki, Hossein Gandomkar","doi":"10.1080/15384101.2025.2575050","DOIUrl":"10.1080/15384101.2025.2575050","url":null,"abstract":"Paclitaxel is a widely used chemotherapeutic agent that plays a vital role in the treatment of various cancers, including breast, ovarian, and lung cancers. Despite its success, the development of resistance significantly limits its long-term efficacy. Paclitaxel resistance involves a range of molecular mechanisms, including alterations in drug transport, mutations in β-tubulin, and activation of pro-survival signaling pathways. Recent studies have highlighted the crucial role of circular RNAs (circRNAs) in mediating paclitaxel resistance. CircRNAs are characterized by their stable, covalently closed structures, which protect them from exonuclease degradation. They regulate drug resistance through various mechanisms, including modulating transcription factors and influencing cellular processes such as apoptosis, immune response, and cancer stem cell dynamics by sponging microRNAs. This review focuses on the mechanisms by which circRNAs contribute to paclitaxel resistance and discusses their dual roles as both oncogenes and tumor suppressors. Furthermore, we explore the potential of circRNAs as novel therapeutic targets to overcome paclitaxel resistance. By targeting specific circRNAs or restoring tumor-suppressive circRNAs, it may be possible to enhance paclitaxel sensitivity and improve treatment outcomes. Future research is essential to further understand the role of circRNAs in paclitaxel resistance and to develop effective circRNA-targeted therapies for cancer treatment.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"422-439"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Construction and validation of predictive model based on endoplasmic reticulum stress-related genes for triple-negative breast cancer. 基于内质网应激相关基因的三阴性乳腺癌预测模型的构建与验证。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-09-01 Epub Date: 2025-09-18 DOI: 10.1080/15384101.2025.2557239

Yongqian Zhang, Hongmin Wang, Lingling Zhu, Xiaojing Chen, Min Zhao, Ming Liu

{"title":"Construction and validation of predictive model based on endoplasmic reticulum stress-related genes for triple-negative breast cancer.","authors":"Yongqian Zhang, Hongmin Wang, Lingling Zhu, Xiaojing Chen, Min Zhao, Ming Liu","doi":"10.1080/15384101.2025.2557239","DOIUrl":"10.1080/15384101.2025.2557239","url":null,"abstract":"Triple-negative breast cancer (TNBC) poses challenges in treatment due to its inherent biological characteristics. Endoplasmic reticulum stress (ERS) has been associated with the development of TNBC. Hence, identifying ERS-related prognostic biomarkers is crucial for the early diagnosis and treatment of TNBC. In this study, we retrieved gene expression profiles from TNBC patients using The Cancer Genome Atlas (TCGA) database. Differentially expressed genes (DEGs) between TNBC tumor and normal tissues were identified using limma package. Using differential expression analysis, we identified 46 ERS-related DEGs. Through univariate Cox, LASSO, and multivariate COX regression analyses, we constructed a prognostic model consisting of 8 genes (IGFBP1, CFTR, THBS4, CREBRF, CLU, HDGF, DERL3, NCCRP1). This model demonstrated robust prognostic accuracy in TNBC patients, validated by the METABRIC dataset. Among the 8 prognostic genes, NCCRP1 showed the highest expression increase in BT-20 and MDA-MB-468 cells. Functional assays further revealed that NCCRP1 significantly promoted proliferation, migration, and invasion, while suppressing apoptosis and ERS in these TNBC cell lines. Our study highlights a strong association between ERS-related genes and the prognosis of TNBC patients. Moreover, we demonstrated that NCCRP1 exerts oncogenic effects in TNBC cells. It provides new insights and possible treatment targets for TNBC.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"350-371"},"PeriodicalIF":3.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12533960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of progression markers for prostate cancer. 前列腺癌进展标志物的鉴定。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-09-01 Epub Date: 2025-09-29 DOI: 10.1080/15384101.2025.2563930

Jie Song, Yang Zhou, Harald Hedman, Tommi Rantapero, Maréne Landström

{"title":"Identification of progression markers for prostate cancer.","authors":"Jie Song, Yang Zhou, Harald Hedman, Tommi Rantapero, Maréne Landström","doi":"10.1080/15384101.2025.2563930","DOIUrl":"10.1080/15384101.2025.2563930","url":null,"abstract":"TGFβ functions as a tumor suppressor or promoter, depending on the context, making TGFβ a useful predictive biomarker. Genes related to TGFβ signaling and Aurora kinase were tested for their ability to predict the progression risk of primary prostate tumors. Using data from The Cancer Genome Atlas (TCGA), we trained an elastic-net regularized Cox regression model including a minimal set of gene expression, copy number (CN), and clinical data. A multi-step feature selection and regularization scheme was applied to minimize the number of features while maintaining predictive power. An independent hold-out cohort was used to validate the model. Expanding from prostate cancer, predictive models were similarly trained on all other eligible cancer types in TCGA. AURKA, AURKB, and KIF23 were predictive biomarkers of prostate cancer progression, and upregulation of these genes was associated with promotion of cell-cycle progression. Extending the analysis to other TCGA cancer types revealed a trend of increased predictive performance on validation data when clinical features were complemented with molecular features, with notable variation between cancer types and clinical endpoints. Our findings suggest that TGFβ signaling genes, prostate cancer related genes and Aurora kinases are strong candidates for patient-specific clinical predictions and could help guide personalized therapeutic decisions.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"382-399"},"PeriodicalIF":3.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12533958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction. 修正。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-09-01 Epub Date: 2025-09-29 DOI: 10.1080/15384101.2025.2534742

引用次数: 0