Cell Cycle最新文献

{"title":"TCAB1: a key promoter of tumor growth through telomere maintenance and senescence evasion.","authors":"Mei-Yu Lin, Dian Jiang, Nini Tian, Xiang Yao, Xing-Hua Pan, Li-Hua Ma, Jing Gao, Zi-An Li, Xiang-Qin Zhu, Xi-Long Zhao, Guang-Ping Ruan","doi":"10.1080/15384101.2025.2609646","DOIUrl":"10.1080/15384101.2025.2609646","url":null,"abstract":"<p><p>TCAB1 (telomerase Cajal body protein 1), encoded by the WRAP53 gene on chromosome 17p13.1, is a molecular scaffold critical for protein-nucleic acid interactions. In normal cells, TCAB1 plays a pivotal role in localizing telomerase to Cajal bodies, thereby ensuring proper telomere maintenance and genomic stability. In cancer cells, however, TCAB1 is frequently overexpressed, which supports unchecked proliferation and therapy resistance. Conversely, knockdown of TCAB1 triggers multiple tumor-suppressive mechanisms, including G1 cell cycle arrest - mediated by impaired p21 ubiquitination and subsequent Cyclin E/CDK2 inactivation - as well as telomere shortening and genomic instability due to mitochondrial dysfunction and defective DNA repair. Notably, the induction of cellular senescence emerges as a key anticancer mechanism upon TCAB1 depletion, particularly in early-stage tumors retaining wild-type p53. This review delineates the dual roles of TCAB1, highlighting its function as a context-dependent oncoprotein and the therapeutic potential of targeting it to induce senescence.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-14"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899224","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}

{"title":"Circular RNA circ_0050102 promotes colorectal cancer progression via modulation of the miR-3622a-3p/BIRC5 signaling pathway.","authors":"Boyang Wang, Bin Zhang","doi":"10.1080/15384101.2025.2592659","DOIUrl":"10.1080/15384101.2025.2592659","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) represents a significant global health burden, requiring a deeper understanding of the molecular mechanisms that drive its progression. Circular RNAs (circRNAs) have appeared as crucial regulators in cancer, with circ_0050102 as a potential functional molecule in CRC. The present study aimed to determine the diagnostic and functional implications of circ_0050102 in CRC pathogenesis.</p><p><strong>Methods: </strong>The GSE172229, GSE205094, and GSE134834 datasets were used for the comprehensive analyses of circRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) in CRC tumor samples. Functional experiments, including fluorescence in situ hybridization, knockdown assays, flow cytometric analysis, and luciferase reporter assay, were conducted to investigate the effect of circ_0050102 on CRC cell behavior. CircRNA - miRNA - mRNA interaction analysis provided information about the regulatory network that involved circ_0050102, miR-3622a-3p, and baculoviral IAP repeat-containing 5 (BIRC5). Furthermore, the functional impact of circ_0050102 on CRC tumor growth was investigated using in vivo xenograft models.</p><p><strong>Results: </strong>Our analysis determined circ_0050102 as a significantly differentially expressed circRNA in CRC, with a high area under the receiver operating characteristic curve value, indicating its diagnostic potential. Functional experiments revealed that circ_0050102 is predominantly localized in the cytoplasm of CRC tumor cells, and its knockdown significantly attenuates various CRC cell behavior aspects, including viability, invasion, and migration (p < 0.05). The interaction analysis revealed a potential regulatory axis that involves circ_0050102, miR-3622a-3p, and BIRC5. In vivo experiments demonstrated that circ_0050102 knockdown significantly attenuated CRC tumor development.</p><p><strong>Conclusion: </strong>Our results revealed that circ_0050102 promotes CRC progression through miR-3622a-3p and BIRC5. The circ_0050102-mediated regulatory network provides valuable information about the intricate mechanisms contributing to CRC pathogenesis.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-19"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888738","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}

{"title":"Microenvironment stiffness regulates cell cycle.","authors":"Shiqi Gu, Yang Yang, Bingxue Lin, Yuwen Luo, Demao Zhang, Jingmei Yang","doi":"10.1080/15384101.2026.2671936","DOIUrl":"10.1080/15384101.2026.2671936","url":null,"abstract":"<p><p>The cell cycle is a highly conserved and ordered process that regulates cell proliferation under physiological and pathological conditions. Among the physical properties of the cellular microenvironment, the extracellular matrix (ECM) stiffness is a crucial regulator of cellular behavior. Emerging research suggests a strong relationship between ECM stiffness and cell cycle progression, although the underlying mechanisms remain unclear. In various diseases, including cancer, neurological disorders, and fibrosis, both ECM stiffness and the cell cycle are tightly involved, thereby influencing disease progression. In addition, ECM stiffness varies across tissues as the disease progresses. This review summarizes current findings on the mechanotransduction pathway through which microenvironmental stiffness regulates the cell cycle across different cell types and stiffness ranges. We also discuss the limitations of the current research and future directions for deepening our understanding of how physical cues in the microenvironment modulate cell cycle control.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-25"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13166190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866871","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}

{"title":"TGFA promotes the development of cervical cancer via interacting with DSG2.","authors":"Chunlin Dong, Bing Zhang, Jing Song, Yaying Lin, Yuan Wang, Jinjin Yu, Ding Ma","doi":"10.1080/15384101.2026.2675355","DOIUrl":"10.1080/15384101.2026.2675355","url":null,"abstract":"<p><p>This study aims to uncover the role and mechanism of transforming growth factor α (TGFA) on the malignant progression of cervical cancer. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to examine the expression levels of TGFA in cancer cells and tissues. Changes in cell viability, apoptosis, and malignant metastatic ability of cancer cells were detected using methylthiazolyldiphenyl-tetrazolium bromide (MTT), flow cytometry, and Transwell method respectively. Autophagy was evaluated via microtubule-associated proteins light chain 3 (LC3) and sequestosome 1 (p62) expression. A nude mouse xenograft model was used for <i>in vivo</i> validation. RNA pull-down assay was performed to explore the interaction between TGFA and desmoglein 2 (DSG2). These results indicated that TGFA expression was elevated in both cervical cancer tissues and cells. TGFA overexpression promoted cell proliferation, metastasis, and autophagy, whereas TGFA knockdown exerted the opposite effects and inhibited tumor growth. Mechanistically, TGFA bound to DSG2 and affected the downstream MYC oncogene (c-MYC)/ADAM metallopeptidase domain 17 (ADAM17) pathway. In conclusion, TGFA serves as an upstream regulator of the DSG2/c-MYC/ADAM17 axis, which is correlated with autophagy and malignant progression of cervical cancer.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-14"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970673","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}

{"title":"Integrated multi-level transcriptomic and bioinformatics analysis identifies lipid metabolism-ubiquitination signatures and reveals ATG5, ASB4, LDLR, and CD36 as Candidate biomarkers in insulin resistance.","authors":"Jicui Chen, Gang Wu, Wei Shi, Xianjun Ma","doi":"10.1080/15384101.2026.2707583","DOIUrl":"10.1080/15384101.2026.2707583","url":null,"abstract":"<p><p>Insulin resistance (IR) is the core pathological basis of type 2 diabetes mellitus (T2DM). This study aimed to identify core lipid metabolism-ubiquitination-related feature genes in IR. Integrative transcriptomic and functional analysis screened differential genes via multiple machine learning models. Gene set enrichment analysis (GSEA), regulatory network prediction, and immune infiltration analysis were performed. C2C12 IR models were constructed, and <i>ATG5</i> was knocked down to detect glucose-lipid metabolism, inflammation, and insulin signaling. Results showed that four feature genes were identified: Good genes Ankyrin Repeat And SOCS Box Containing 4 (<i>ASB4)</i>/ Low Density Lipoprotein Receptor (<i>LDLR)</i> and Bad genes <i>ATG5</i>/ CD36 molecule (CD36 blood group) (<i>CD36)</i>. They were enriched in metabolism/inflammation pathways consistent with IR phenotypes. Regulatory network analysis predicted potential upstream microRNAs (miRNAs) and transcription factors (TFs) modulating these feature genes. IR/diabetes groups had lower ImmuneScores vs. insulin-sensitive groups. <i>ATG5</i> was upregulated in IR models. Its knockdown inhibited autophagy, improved glucose and lipid metabolism, decreased inflammatory cytokines, and exerted no influence on cell viability. In conclusion, <i>ASB4</i>, <i>LDLR</i>, <i>ATG5</i>, and <i>CD36</i> are potential IR biomarkers. <i>ATG5</i> regulates IR via autophagy, insulin signaling, and metabolism, serving as a therapeutic target for metabolic diseases.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-27"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13418714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590564","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}

{"title":"From single-pathway reporters to integrated sensors: molecular imaging challenges in detecting PANoptosis.","authors":"Kulsoom, Wajahat Ali, Latofatoy Nurislomova, Gulmira Ibrohimova, Otabek Kuziev, Jumaniyozov Kuvondik, Jasurbek Mamajonov","doi":"10.1080/15384101.2026.2735513","DOIUrl":"10.1080/15384101.2026.2735513","url":null,"abstract":"<p><p>PANoptosis is an integrated inflammatory cell death program that arises from the coordinated activation of apoptotic, pyroptotic, and necroptotic signaling pathways. Although it is increasingly recognized as a central determinant of immune defense, therapeutic response, and disease progression, PANoptosis remains largely undetectable using current molecular imaging and detection strategies. Most existing molecular probes are designed to interrogate individual cell death pathways, typically apoptosis, thereby reducing a multidimensional execution network to a single biochemical readout. Here, we critically examine why conventional cell death probes fail to resolve PANoptosis and systematically categorize current sensing strategies according to their apoptotic, pyroptotic, and necroptotic targets. We further highlight emerging multiplexed, logic-gated, and nanoplatform-based sensing architectures that partially address these limitations but remain mechanistically incomplete. Building on current insights into PANoptosome biology, we propose a set of design principles for next-generation PANoptosis probes that emphasize multi-axis molecular integration, temporal resolution, and conditional activation logic. By reframing PANoptosis as a measurable biological state rather than a conceptual abstraction, this review provides a roadmap for developing molecular probes capable of decoding inflammatory cell death in complex diseases. Such advances will be essential for translating PANoptosis from mechanistic insight into diagnostic and therapeutic applications.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-32"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104620","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}

{"title":"Mitotic error correction and the spindle assembly checkpoint: a tension-filled relationship.","authors":"Richard Pleuger, Stefan Westermann","doi":"10.1080/15384101.2026.2653527","DOIUrl":"10.1080/15384101.2026.2653527","url":null,"abstract":"<p><p>The fidelity of mitotic chromosome segregation relies on kinetochores detecting sister chromatid bi-orientation to control error correction (EC) and the spindle assembly checkpoint (SAC). The kinetochore-microtubule attachment state needs to be decoded, the signal processed, and transduced, resulting in either stabilization or destabilization of the attachment. Although many crucial players of this process have been identified, the molecular mechanisms underlying signal integration remain an open question. Focusing on the model system <i>Saccharomyces cerevisiae</i>, we explore the interdependent contributions of the conserved protein kinases Mps1 and Ipl1^{Aurora B}, crucial regulators of mitotic chromosome segregation. We discuss how bi-orientation reorganizes the kinetochore attachment site and we present a perspective on how these structural changes can alter kinase localization and activity.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-19"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608213","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}

{"title":"Identification of mitochondrial permeability transition-related gene signatures to predict lung adenocarcinoma survival and drug response.","authors":"Lin Liu, Mingjun Gao, Wenbo He, Mengmeng Wang, Siding Zhou, Xiaolin Wang, Yusheng Shu","doi":"10.1080/15384101.2025.2606113","DOIUrl":"10.1080/15384101.2025.2606113","url":null,"abstract":"<p><p>This study investigated mitochondrial permeability transition-driven necrosis-related genes (MPTDNRGs) and its association with lung adenocarcinoma (LUAD). We systematically investigated their genetic variation, expression patterns, and prognostic value. A risk prediction model for MPTDNRGs was contrasted using Cox regression and least absolute shrinkage and selection operator regression analyses. MPTDNRG scores were used to quantify LUAD subtypes. We evaluated their value in the tumor microenvironment (TME), tumor mutational burden (TMB), prognostic prediction, and drug sensitivity in LUAD. The expression level, copy number variation, methylation, and microRNA (miRNA) status of PSMB7 were analyzed. We also analyzed the expression and knockdown efficiency of PSMB7 in LUAD by immunohistochemical staining, real-time fluorescence quantitative polymerase chain reaction, and western blotting. PSMB7 function in LUAD cells and in vivo was assayed using Cell Counting Kit 8, colony formation, wound healing, Transwell assays, flow cytometry, and mouse models. Seven MPTDNRG features were successfully constructed to predict LUAD prognosis and validated in an external cohort. Patients were categorized into high- and low-risk groups based on risk scores. The high-risk group exhibited shorter survival times, lower TME scores, weaker TME cell infiltration, and higher TMB scores than the low-risk group. Cancer stem cell index, mutation frequency, and drug sensitivity significantly differed between the two groups. MPTDNRG score could independently predict LUAD. PSMB7 was highly expressed in various tumors, and copy number variation, methylation, and miRNA expression significantly differed among different cancers. PSMB7 was highly expressed in LUAD tissues and cell lines. PSMB7 knockdown inhibited cancer cell proliferation, migration, invasion, and epithelial - mesenchymal transition, and promoted apoptosis. PSMB7 exerted tumorigenic effects in mice. In conclusion, we comprehensively demonstrated the characterization of MPTDNRGs in LUAD and constructed a new risk prediction model. Meanwhile, PSMB7 was shown to be a possible new target for LUAD treatment.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-35"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848968","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}

{"title":"Exosomes derived from AHR-overexpressing human umbilical cord mesenchymal stem cells attenuate H/R injury via AHR/NLRP3 pathway.","authors":"Ying Qin, Dongyan Shen, Kequan Guo, Xu Meng, Xiaozheng Cui, Yongchao Li, Yixin Jia","doi":"10.1080/15384101.2025.2609649","DOIUrl":"10.1080/15384101.2025.2609649","url":null,"abstract":"<p><p>Myocardial hypoxia-reoxygenation (H/R) injury is a frequently observed pathological event in various cardiovascular conditions. Despite the therapeutic promise of human umbilical cord mesenchymal stem cells (hUC-MSCs) in alleviating myocardial damage, their clinical use faces obstacles such as limited implantation efficiency, poor retention, and reduced post-transplantation viability. Exosomes secreted by hUC-MSCs have emerged as a viable alternative, potentially addressing these challenges. Nonetheless, the underlying mechanisms through which these exosomes confer cardioprotection have yet to be fully elucidated. This study aims to explore the protective effect of hUC-MSCs exosomes on myocardial H/R injury via the aryl hydrocarbon receptor (AHR)/NOD-like receptor family pyrin domain containing 3 (NLRP3) pathway and to assess their impact on immune cell phenotype conversion. hUC-MSCs exosomes significantly upregulated AHR expression, inhibited NLRP3-related inflammatory protein expression, enhanced myocardial cell survival, and reduced apoptosis. The protective effect of hUC-MSCs exosomes was abolished following AHR knockdown. Additionally, exosomes from AHR-overexpressing hUC-MSCs promoted the conversion of macrophages, dendritic cells (DCs), and T cells to an anti-inflammatory phenotype, thereby further enhancing myocardial protection. These findings indicted that exosomes from AHR-overexpressing hUC-MSCs protect myocardium via AHR/NLRP3 signaling, improving immune microenvironment and offering new therapeutic potential.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-22"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164291","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}

{"title":"MAGED4 promotes hepatocellular carcinoma progression via activation of JAK2/STAT3 pathway by stabilizing TRIM21.","authors":"Yipu Zhao, Yi Zhang, Jiahui Cao, Zhipu Liu, Rongtao Zhu, Ruopeng Liang, Weijie Wang, Jian Li, Yuling Sun","doi":"10.1080/15384101.2026.2685807","DOIUrl":"10.1080/15384101.2026.2685807","url":null,"abstract":"<p><p>Melanoma-associated antigen D4 (MAGED4) belongs to the melanoma-associated antigen family and is upregulated in various cancer types. However, the functional role and molecular mechanisms of MAGED4 in hepatocellular carcinoma (HCC) remain largely unknown. In this study, we observed that MAGED4 expression levels were significantly higher in HCC tissues than in non-cancerous tissues and elevated expression was associated with poor patient outcomes. Functional assays demonstrated that MAGED4 promoted proliferation and migration of HCC. We found that MAGED4 can activate the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Mass spectrometry and co-immunoprecipitation assays revealed an interaction between MAGED4 and tripartite motif-containing 21 (TRIM21). Confocal microscopy experiments confirmed the colocalization of MAGED4 with TRIM21. Mechanistically, MAGED4 can regulate the stability of TRIM21 by preventing its ubiquitination and degradation. Furthermore, MAGED4 contributes to the downregulation of suppressor of cytokine signaling 3 (SOCS3) via TRIM21, and this effect can be partially reversed by si-TRIM21 in MAGED4-overexpressing cells. These findings indicate that MAGED4 promotes HCC progression through the activation of the JAK2/STAT3 pathway by stabilizing TRIM21, suggesting that targeting MAGED4 may provide new insights into HCC treatment strategies.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-15"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216627","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}