Cellular Oncology最新文献

{"title":"ENY2 transcription and export complex 2 subunit deficiency induces nucleolar stress to inhibit tumor progression through NPM1/MDM2/p53-dependent and -independent responses.","authors":"Shiqi Zuo, Siyuan He, Zhiqin Zhu, Yanjie Hou, Ziqing Wu, Yao Tang, Yujiao Zou","doi":"10.1007/s13402-025-01148-4","DOIUrl":"10.1007/s13402-025-01148-4","url":null,"abstract":"<p><strong>Purpose: </strong>The selective induction of nucleolar stress in cancer cells has become a potential anticancer therapy. However, precisely regulating the key molecules involved in nucleolar stress remains a challenging topic in current research. ENY2 transcription and export complex 2 subunit (ENY2) is a transcription-associated nuclear protein that is upregulated in several cancers. However, its specific function and mechanistic role in oncogenesis remain poorly characterized and require further exploration.</p><p><strong>Methods: </strong>ENY2 was identified by screening ChIP-seq and public databases. Its role in tumor development was confirmed through in vivo and in vitro experiments. RNA sequencing, polysome profiling, agarose gel electrophoresis, and immunofluorescence suggested ENY2's involvement in ribosome biogenesis. Interacting proteins were identified by confocal microscopy, co-IP, and molecular docking, then validated by western blotting and ubiquitination assays. Finally, drug resistance experiments evaluated ENY2's clinical potential.</p><p><strong>Results: </strong>We discovered that the overexpression of ENY2 significantly enhances tumor growth and cell cycle progression both in vitro and in vivo. Conversely, depletion of ENY2 facilitating the release of NPM1 into the nucleoplasm, thereby impeding ribosomal subunit export and inducing nucleolar stress. Additionally, the released NPM1 interacts with MDM2 within the nucleus to stabilize p53 protein levels, consequently inhibiting tumor growth. Notably, knockdown of ENY2 in p53-mutant cancer cell lines exhibits an augmented binding affinity and silencing efficacy of RISC towards target mRNA molecules, ultimately suppressing tumor proliferation through a p53-independent manner.</p><p><strong>Conclusions: </strong>This study elucidated a previously unrecognized role of ENY2 in tumor growth, clarified the NPM1/MDM2/ p53-dependent mechanism of ENY2-mediated tumor cell growth suppression. We also provided a novel p53-independent RISC-IL11 nucleolar stress response pathway, which may provide a new target for the treatment of breast cancer.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"41"},"PeriodicalIF":4.8,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12876109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding SR protein regulation: kinases, phosphatases, and therapeutic targeting strategies.","authors":"Nasi Liu, Fleur van der Ende, Bob van de Water, Sylvia E Le Dévédec","doi":"10.1007/s13402-026-01168-8","DOIUrl":"10.1007/s13402-026-01168-8","url":null,"abstract":"<p><p>RNA splicing is a fundamental cellular process that transforms precursor messenger RNA (pre-mRNA) into mature messenger RNA (mRNA) by removing non-coding introns and rejoining coding exons. Serine/arginine-rich (SR) proteins, a family of RNA-binding proteins, play crucial roles in RNA splicing by recruiting essential components for spliceosome assembly. The activity of SR proteins is tightly regulated by post-translational modifications, including phosphorylation, acetylation, methylation, and ubiquitination. Among these, the dynamic balance between phosphorylation and dephosphorylation is particularly critical for modulating SR protein function. Given their involvement in cancer, SR proteins represent promising targets for therapeutic intervention. In this review, we provide a comprehensive overview of the current understanding of the regulatory networks involving kinases and phosphatases governing SR protein phosphorylation. We also discuss the existing therapeutic strategies using small-molecule inhibitors aimed at regulating SR protein phosphorylation in the context of cancer. In conclusion, this review highlights the importance of phosphorylation regulation in SR protein function and the RNA splicing process. Targeting SR protein phosphorylation may open new therapeutic avenues or enhance the efficacy of cancer treatments when used in combination with other drugs.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"40"},"PeriodicalIF":4.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intratumoral PD-1^high CD8⁺ T cells correlate with AFP levels in HCC patients: a brief report.","authors":"Zuzana Macek Jilkova, Julien Ghelfi, Lucile Dumolard, Christian Sengel, Bleuenn Brusset, Yann Teyssier, Charlotte Costentin, Thomas Decaens","doi":"10.1007/s13402-026-01170-0","DOIUrl":"10.1007/s13402-026-01170-0","url":null,"abstract":"<p><p>PURPOSE: Hepatocellular carcinoma (HCC), the most common primary liver cancer, typically arises in a context of chronic inflammation driven by metabolic dysfunction, long-term alcohol use, viral hepatitis, and other etiologies. This study aimed to investigate whether intrahepatic and circulating immune profiles in HCC patients correlate with patient characteristics or clinical parameters. METHODS: Fresh tumor tissue, paired non-tumor liver tissue, and peripheral blood samples from 93 patients with HCC were analyzed using multiparametric flow cytometry to characterize lymphocyte subsets (T cells, NK cells, NKT cells, and B cells), immune checkpoint molecule expression (ICOS, 4-1BB, OX40, PD-1, TIM-3, LAG-3, and CTLA-4), and activation status. Associations between immune parameters and patient demographic or clinical features were assessed. RESULTS: Circulating alpha-fetoprotein (AFP) levels positively correlated with tumor-infiltrating PD-1high CD8+ T cell frequency (r=0.45, p<0.0001), but this correlation was not observed in non-tumoral or circulating compartments. CONCLUSION: AFP-producing HCC is linked to intra-tumoral immune exhaustion, marked by PD-1high CD8+ T cell accumulation, suggesting a localized immunosuppressive effect mediated by tumor-secreted AFP. </p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"39"},"PeriodicalIF":4.8,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12868040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural-tumor crosstalk and molecular targeting: mechanisms and therapeutic implications in cancer neuroscience.","authors":"Tianhui Hou, Huaze Ding, Guofang Huang, Tong Meng, Dianwen Song","doi":"10.1007/s13402-025-01151-9","DOIUrl":"10.1007/s13402-025-01151-9","url":null,"abstract":"<p><p>The nervous system is increasingly recognized as a key regulator of the tumor microenvironment, engaging in bidirectional crosstalk with cancer cells through neurotransmitters, neuropeptides, and synaptic-like connections. Autonomic nerves modulate tumor progression: sympathetic signaling promotes growth, metastasis, and immune evasion via β-adrenergic receptor activation, while parasympathetic input exerts dual roles—driving gastric cancer yet protecting against colitis-associated colorectal cancer through the cholinergic anti-inflammatory pathway. Sensory nerves influence pain, angiogenesis, and immunity, with CGRP and substance P differentially regulating anti-tumor responses. Notably, functional neuro-glioma synapses have been identified, where neuronal glutamate release activates AMPA receptors on tumor cells, triggering Ca²⁺ influx and oncogenic signaling—providing a mechanistic basis for repurposing AMPA antagonists like perampanel. Glial cells, including Schwann cells and astrocytes, support perineural invasion, metabolic coupling, and therapy resistance via neurotrophic factor secretion and extracellular matrix remodeling. Tumor-derived signals reciprocally rewire neural circuits, enhancing innervation and neuroplasticity. Central brain regions, such as the paraventricular nucleus, integrate stress inputs to systemically regulate tumor immunity and metabolism through autonomic output. This dynamic interplay positions the nervous system as a master regulator of cancer biology. Targeting neural-tumor interactions—via β-blockers, neuromodulation, or bioelectronic medicine—offers novel therapeutic strategies. Future precision oncology approaches must consider tumor type, stage, and neural context to effectively disrupt this crosstalk and the emerging concept of cancer-induced nerve injury (CINI) as a novel mechanism of immunotherapy resistance.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"35"},"PeriodicalIF":4.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL1-mediated m⁷G tRNA modification promotes colorectal cancer progression and liver metastasis via translational regulation.","authors":"Jiale Chen, Gaomin Zheng, Yixi Wen, Fei Fang, Yuyao Liu, Ziqin Liu, Tianhong Su, Shuibin Lin, Shumin Li, Junbin Liao, Lixia Xu, Guopei Zhang, Manling Huang, Beifang Li","doi":"10.1007/s13402-025-01137-7","DOIUrl":"10.1007/s13402-025-01137-7","url":null,"abstract":"<p><p>BACKGROUND: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with colorectal cancer liver metastasis (CRLM) being the primary cause of death. Despite its clinical significance, the molecular mechanisms underlying CRC progression remain poorly understood. METHODS: Unbiased proteomic profiling and single-cell RNA sequencing (scRNA-seq) analyses of CRC tissues from patients with and without liver metastases identified methyltransferase-like protein 1 (METTL1) as a critical regulator, with its function in CRC progression validated through in vitro and in vivo gain- and loss-of-function studies. Furthermore, tRNA methylation sequencing (TRAC-seq) and ribosome-nascent chain complex sequencing (RNC-seq) were performed to investigate the downstream mechanisms. RESULTS: METTL1 was significantly elevated in CRC, with the highest expression in CRLM, and correlated with poor survival. METTL1 knockout inhibited tumor cell proliferation, migration, and invasion in vitro, whereas overexpression of wild-type METTL1, but not its catalytically inactive mutant, promoted oncogenic phenotypes. Consistently, METTL1 knockout attenuated tumor growth and liver metastasis in vivo. Mechanistically, METTL1-mediated m7G tRNA modification selectively enhanced translation of oncogenic transcripts, particularly those involved in cell cycle regulation (e.g., CCND3) and PI3K/Akt signaling. Notably, forced CCND3 expression partially rescued the phenotypes induced by METTL1 knockout. CONCLUSIONS: Our findings highlight the crucial role of METTL1 and its tRNA m7G modification in promoting CRC progression and liver metastasis, providing promising targets for therapy in advanced CRC. </p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"38"},"PeriodicalIF":4.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CXCL12 derived from cancer-associated fibroblasts mediates dysfunctional intratumoral adaptive immunity in diabetic pancreatic adenocarcinoma.","authors":"Jialun Wang, Yue Zhou, Xiaoxuan Han, Yihan Zhao, Aotian Chen, Yu Chen, Shu Zhang, Ying Lv, Lei Wang","doi":"10.1007/s13402-026-01165-x","DOIUrl":"10.1007/s13402-026-01165-x","url":null,"abstract":"<p><p>BACKGROUND: Diabetes mellitus (DM) affects the occurrence and progression of pancreatic adenocarcinoma (PAAD), but the DM-related immune characteristic in PAAD remains unclear. This study aimed to elucidate the immune landscape and underlying mechanism in diabetic PAAD. METHODS: RNA-sequencing data from primary sorted cancer-associated fibroblasts (CAFs) and TCGA database were used to screen out differentially expressed genes (DEGs), and enrichment analyses were performed to identify key pathways. xCell, Timer, Estimate, Quantiseq, and MCPcounter algorithms were applied to assess intratumoral immune infiltration, which was meanwhile verified by multicolor immunofluorescence of clinical samples. In vitro experiments, including proliferation assay and immune phenotype identification, were carried out to confirm the impact of the key gene on immune reprogramming. An animal model of mixed injection of pancreatic stellate cells (PSCs) and pancreatic cancer cells was constructed to validate in vivo effects of involved pathway in diabetic pancreatic cancer. RESULTS: Screened DEGs were enriched in several immunomodulatory pathways. The immunity in diabetic pancreatic cancer was shown to be seemingly flourishing but functionally defective, characterized by CD22+ B cells and TIGIT+ CD8+ T cells. Correlation analyses indicated that CXCL12 was significantly associated with the abundance and immune phenotype transformation of B and CD8+ T cells, with consistent results across multiple algorithms. More CXCL12High CAFs were detected in diabetic PAAD patients and mice. Meanwhile, the treatment of CXCL12High PSCs promoted the immune-suppressive phenotype of B and CD8+ T cells in both in vitro and in vivo experiments, and the blockade of CXCL12–CXCR4 axis by plerixafor showed therapeutic effects in subcutaneous tumor models. CONCLUSIONS: Our results delineated a distinct immune-suppressive landscape mediated by CAF-derived CXCL12 in diabetic PAAD individuals, which may help guide treatment decisions and predict immunotherapy response. </p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"36"},"PeriodicalIF":4.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Unraveling the impact of cancer-associated fibroblasts on lymphatic metastasis of head and neck squamous cell carcinoma.","authors":"Zunxuan Xie, Boyang Gao, Han Wu, Fang Zheng, Qinglong Song, Cangwei Liu, Ce Shi","doi":"10.1007/s13402-026-01169-7","DOIUrl":"10.1007/s13402-026-01169-7","url":null,"abstract":"","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"37"},"PeriodicalIF":4.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The moonlighting functions of glycolytic enzymes in tumorigenesis.","authors":"Xin Chen, Jing Yang, Yongjun Ma","doi":"10.1007/s13402-025-01135-9","DOIUrl":"10.1007/s13402-025-01135-9","url":null,"abstract":"<p><p>Glycolysis is a ubiquitous energy-supply process that occurs in virtually all living cells. The phenomenon of aerobic glycolysis, known as the Warburg effect, is observed and considered as a hallmark of tumorigenesis. However, the roles and unresolved mechanisms of glycolytic enzymes in cancer progression remain incompletely understood. In this review, we synthesize emerging knowledge on the non-glycolytic (“moonlighting”) functions of key glycolytic enzymes in tumorigenesis, which are independent of their canonical catalytic activity and enable them to govern diverse cellular processes beyond energy metabolism. We also discuss their potential as therapeutic targets and establish a conceptual framework for understanding how these moonlighting activities govern tumor progression, thereby supporting the development of novel anticancer therapies.Clinical trial numberNot applicable.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"34"},"PeriodicalIF":4.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akt/mTOR pathway-mediated CCNA1 regulation of radiotherapy resistance in nasopharyngeal carcinoma.","authors":"Ruifang Zeng, Liting Zhong, Pengfei Li, Xiaoying Gao, Yanfeng Chen, Wenwen Hao","doi":"10.1007/s13402-026-01166-w","DOIUrl":"10.1007/s13402-026-01166-w","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC), as a cancer type highly sensitive to radiotherapy, has radiation therapy as the preferred clinical treatment strategy. However, acquired radioresistance poses a significant challenge to the overall therapeutic efficacy for NPC patients.</p><p><strong>Methods: </strong>In this study, we established two radioresistant NPC cell lines, CNE2-IR and HONE1-IR.</p><p><strong>Results: </strong>RNA sequencing analysis revealed that CCNA1 was upregulated in both radioresistant NPC cell lines. Downregulation of CCNA1 enhanced the radiosensitivity of these two radioresistant NPC cell lines. Further research found that CCNA1 expression was induced and upregulated during radiotherapy and was associated with poor prognosis in NPC patients. Through in-depth mechanistic studies, we confirmed that CCNA1 may influence radiosensitivity through ROS antioxidant stress and anti-apoptotic signaling. High expression of CCNA1 enhanced NPC cell viability and inhibited apoptosis, while downregulating CCNA1 improved the radiosensitivity of NPC cells. The mechanism of radiosensitization was primarily mediated by the AKT/mTOR pathway.</p><p><strong>Conclusions: </strong>These findings suggest that CCNA1 could serve as a potential predictive biomarker for radiosensitivity in NPC patients, providing new insights for developing personalized comprehensive chemoradiotherapy strategies for NPC patients.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"32"},"PeriodicalIF":4.8,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12852267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulated ARMCX1 suppresses nasopharyngeal carcinoma progression by promoting TRIM21-mediated β-catenin degradation.","authors":"Zhe Hu, Enqing Zhuo, Jiankang Guo, Yilin Wu, Xiaoou Sun, Houkuang Qiu, Yangfan Zhou, Xi Tan, Xuhui Zhang","doi":"10.1007/s13402-025-01161-7","DOIUrl":"10.1007/s13402-025-01161-7","url":null,"abstract":"<p><p>BACKGROUND: Armadillo repeat-containing X-linked 1 (ARMCX1) has been reported to exhibit a suppressive effect in a variety of solid tumors. However, neither its biological role nor its potential mechanism of action has yet been reported in nasopharyngeal carcinoma (NPC). METHODS: Immunohistochemical staining of an NPC tissue microarray was performed to evaluate the clinicopathologic association between ARMCX1 and NPC patients. The effect of ARMCX1 on the growth, migratory, and invasive capacities of NPC cells was assessed in vitro using colony formation, Cell Counting Kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), scratch, and Transwell assays. A subcutaneous graft tumor model was implemented to investigate the impact of ARMCX1 on the tumor growth of NPC cells in vivo. Western blotting, immunofluorescence staining, and cycloheximide and proteasome inhibitor experiments were employed to investigate the potential molecular mechanisms of ARMCX1 in NPC RESULTS: Overexpression of ARMCX1 effectively inhibited the growth, migration, and invasion in NPC cells. Western blotting, co-immunoprecipitation, immunofluorescence, and cycloheximide and proteasome inhibitor experiments revealed that ARMCX1 mediated the β-catenin ubiquitination and degradation via recruiting tripartite motif-containing protein 21 (TRIM21), thereby suppressing cell cycle progression and epithelial–mesenchymal transition. Final rescue assays demonstrated that β-catenin reversed ARMCX1-mediated suppression of NPC cell proliferation, migration, and invasion. CONCLUSIONS: ARMCX1 attenuates NPC cell proliferation, migration, and invasion by binding β-catenin and promoting its ubiquitination-dependent degradation via TRIM21. Hence, ARMCX1 may serve as a potential molecular target for therapeutic intervention in NPC. </p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":"49 1","pages":"25"},"PeriodicalIF":4.8,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12804310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}