Cell Biochemistry and Function最新文献

Overview on Epstein–Barr Virus–Host Interactions With a Focus on Host Cell Transcriptome Alterations Epstein-Barr病毒与宿主相互作用的综述，重点是宿主细胞转录组的改变。

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-14 DOI: 10.1002/cbf.70322

Louise Wallot, Tim Hohmann, Urszula Hohmann, Faramarz Dehghani, Olaf Grisk, Simon Jasinski-Bergner

{"title":"Overview on Epstein–Barr Virus–Host Interactions With a Focus on Host Cell Transcriptome Alterations","authors":"Louise Wallot, Tim Hohmann, Urszula Hohmann, Faramarz Dehghani, Olaf Grisk, Simon Jasinski-Bergner","doi":"10.1002/cbf.70322","DOIUrl":"10.1002/cbf.70322","url":null,"abstract":"The Epstein–Barr virus (EBV) belongs to the gamma subgroup of human herpesviruses. EBV is particularly lymphotropic regarding its latency, meaning that it preferentially targets lymphocytes as its immunological niche. During the establishment of the complex virus–host relationships, the virus influences the human host cell transcriptome inducing changes in RNA quantity and quality aided by a multitude of virally encoded molecules such as microRNAs, lncRNAs, peptides, and proteins. Quantitative changes in human gene expression of infected host cells are due to epigenetic mechanisms, such as altered promoter methylation patterns and altered microRNA- or lncRNA-based post-transcriptional gene regulation mechanisms. The quality of the human transcriptome is altered including changes in chemical RNA modifications and alterations in alternative splicing (AS) patterns. These molecular mechanisms contribute to the immune evasion of EBV, enhanced host cell proliferation and desensitization to apoptosis induction. These mechanisms are highly relevant to the process of malignant transformation of infected host cells, highlighting the tumorigenic potential of EBV. This review article addresses the role of AS in malignant transformation of EBV-infected host cells. For this purpose, publicly available transcriptome datasets from EBV-positive human Burkitt lymphomas (BL) were analyzed in an EBV-copy number dependent manner. We identified 14 directly dysregulated splicing factors, predominantly components of the splicing machinery as well as trans-acting splicing factors, with putative relevance for virus-mediated alterations of host cell splicing patterns.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179530","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

Recent Advances in Research on SHP Family Phosphatases: Signal Regulation Mechanisms and Disease Associations SHP家族磷酸酶的信号调控机制及其与疾病的关系研究进展

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-14 DOI: 10.1002/cbf.70315

Xuebin Li, Xiaoqing Duan, Nanxiu Liu, Wangjie Tang, Yi He, Dongsheng Zhou, Jianguo Yan, Yali Zhou

{"title":"Recent Advances in Research on SHP Family Phosphatases: Signal Regulation Mechanisms and Disease Associations","authors":"Xuebin Li, Xiaoqing Duan, Nanxiu Liu, Wangjie Tang, Yi He, Dongsheng Zhou, Jianguo Yan, Yali Zhou","doi":"10.1002/cbf.70315","DOIUrl":"10.1002/cbf.70315","url":null,"abstract":"The protein tyrosine phosphatase family comprises a large number of members. Among them, Src homology 2 (SH2) domain-containing protein tyrosine phosphatases (commonly referred to as the SHP family). Members of the SHP family regulate multiple signaling pathways by catalyzing the dephosphorylation of substrate proteins, thereby participating in fundamental biological processes such as immune regulation and cell proliferation. Their normal function is essential for maintaining organismal homeostasis. Extensive evidence indicates that dysregulation of SHP family members is closely associated with a variety of diseases. Accordingly, this review summarizes the functional characteristics of SHP-1 and SHP-2, with particular emphasis on advances in their structural regulation, substrate recognition, signaling pathway regulation, and disease-related mechanisms. It further discusses key controversies and unresolved scientific questions concerning SHP family regulation, as well as recent advances in targeted therapeutic strategies, thereby contributing to a deeper understanding of SHP family biology and informing the development of precision therapies.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179567","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

HBQ1 Acts as a Prognostic Biomarker and Tumor Suppressor Linked to Antigen Presentation in Glioma HBQ1在胶质瘤中作为与抗原呈递相关的预后生物标志物和肿瘤抑制因子。

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-13 DOI: 10.1002/cbf.70323

Cheng Xie, Qinglin Zhong, Mingang Zou, Qianliang Huang, Lukui Chen, Wenjin Wei

{"title":"HBQ1 Acts as a Prognostic Biomarker and Tumor Suppressor Linked to Antigen Presentation in Glioma","authors":"Cheng Xie, Qinglin Zhong, Mingang Zou, Qianliang Huang, Lukui Chen, Wenjin Wei","doi":"10.1002/cbf.70323","DOIUrl":"10.1002/cbf.70323","url":null,"abstract":"Glioma is a highly aggressive brain tumor associated with substantial morbidity and mortality and with limited treatment options. This study investigates the functional role of Hemoglobin Subunit Theta 1 (HBQ1) in glioma and evaluates its potential as a prognostic biomarker. Using integrated bioinformatics approaches, we demonstrated that HBQ1 expression was significantly downregulated in glioma tissues compared to normal brain tissues and was inversely correlated with tumor grade. Survival analysis indicated that lower HBQ1 expression is associated with poorer overall survival and disease-free survival. Functional enrichment analyses connected HBQ1 to key pathways including antigen presentation (MHC II), calcium signaling, mitogen‑activated protein kinase (MAPK) signaling, and γ‑aminobutyric acid (GABA)‑ergic synapse. In vitro, overexpression of HBQ1 in U87 cells markedly suppressed proliferation, migration, and invasion, while enhancing antigen presentation. Moreover, HBQ1 expression was significantly correlated with important molecular markers such as isocitrate dehydrogenase (IDH) mutation, 1p/19q co-deletion, and O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation, as well as with genes involved in glutamate-GABA metabolism. Collectively, our findings identify HBQ1 as a novel prognostic biomarker and a potential tumor suppressor in glioma, possibly through modulating the immune microenvironment and neuron–glioma crosstalk.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179594","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

Exosomal let-7c-5p From AMI Patient Plasma Modulates Neuronal PANoptosis via ZBP1 In Vitro AMI患者血浆外泌体let-7c-5p通过ZBP1体外调节神经元PANoptosis

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-08 DOI: 10.1002/cbf.70318

Zhiyong Zhang, Shaohan Zhang, Yuzhi Shao, Zhiguang Wang, Lei Yan, Xinyu Wang, Wei Li, Kerui Gong, Gang Fu, Jie Yan, Wendian Yang, Guo Shao

{"title":"Exosomal let-7c-5p From AMI Patient Plasma Modulates Neuronal PANoptosis via ZBP1 In Vitro","authors":"Zhiyong Zhang, Shaohan Zhang, Yuzhi Shao, Zhiguang Wang, Lei Yan, Xinyu Wang, Wei Li, Kerui Gong, Gang Fu, Jie Yan, Wendian Yang, Guo Shao","doi":"10.1002/cbf.70318","DOIUrl":"10.1002/cbf.70318","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 Acute myocardial infarction (AMI) significantly elevates the risk of ischemic stroke (IS), yet the molecular mechanisms linking cardiac and cerebral injury remain unclear. Emerging evidence highlights the role of circulating exosomes in mediating inter-organ communication via microRNAs (miRNAs). In this study, plasma exosomes from AMI patients were isolated at three time points (before, 2 hours after, and 24 hours after reperfusion therapy (RT)), and the exosomal let-7c-5p level was measured. The effects of plasma exosomes on neuronal SH-SY5Y cells under normoxic and oxygen-glucose deprivation (OGD) conditions were evaluated by assessing cell viability and the Z-DNA binding protein 1 (ZBP1)/PANoptosis pathway using CCK-8 assay and western blot analysis. let-7c-5p was overexpressed to clarify its role in the ZBP1/PANoptosis pathway. Exosomal let-7c-5p from AMI patients showed differences at three time points. Exosomes collected before reperfusion therapy induced the most PANoptosis under normal conditions, whereas those collected 2 hours post-reperfusion therapy had the greatest effect under OGD. These effects correlated with dynamic changes in exosomal let-7c-5p levels and the expression of ZBP1. Let-7c-5p overexpression reduced ZBP1 and PANoptotic markers, suggesting a neuroprotective role under ischemic stress. Our study suggested that the exosomal let-7c-5p/ZBP1/PANoptosis axis may contribute to AMI-related brain injury, offering potential therapeutic targets for intervention.\u0000 </section>\u0000 </div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70318","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135185","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

Zinc Finger Protein 143 Bidirectionally Regulates the Proliferation of Hepatocytes and Hepatocellular Carcinoma Cells via c-Myc 锌指蛋白143通过c-Myc双向调控肝细胞和肝癌细胞的增殖

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-07 DOI: 10.1002/cbf.70320

Caifang Sun, Meijuan Yue, Yuxiang Chen, Jiaying Zhang, Yunyun Mai, Yuhang Zhang, Bingyu Ye

{"title":"Zinc Finger Protein 143 Bidirectionally Regulates the Proliferation of Hepatocytes and Hepatocellular Carcinoma Cells via c-Myc","authors":"Caifang Sun, Meijuan Yue, Yuxiang Chen, Jiaying Zhang, Yunyun Mai, Yuhang Zhang, Bingyu Ye","doi":"10.1002/cbf.70320","DOIUrl":"https://doi.org/10.1002/cbf.70320","url":null,"abstract":"The transcription factor zinc finger protein 143 (ZNF143) plays a crucial role in regulating diverse biological processes, including cell cycle progression, development, and cellular differentiation. Similarly, c-Myc is well-established as a key regulator of cell proliferation, differentiation, and metabolic homeostasis. While studies have demonstrated ZNF143's involvement in the proliferation of both normal hepatocytes and hepatoma cells, the precise mechanisms underlying ZNF143-mediated regulation of hepatocyte proliferation, as well as its potential functional interplay with c-Myc in this process, remain to be fully elucidated. In this study, we investigated the dynamic expression patterns of ZNF143 and c-Myc during distinct phases of liver regeneration using a 2/3 partial hepatectomy (PHx) mouse model. To elucidate the regulatory roles of these factors in hepatocyte proliferation, we employed the mouse normal hepatocyte line AML12 and the human hepatoma cell line Huh7 as experimental models. Through MTT, CCK-8, EdU, quantitative real-time PCR (qRT-PCR), and Western blot, we examined the individual and combined effects of ZNF143 and c-Myc on hepatocyte proliferation. Our findings reveal that ZNF143 inhibits proliferation and cell cycle progression in AML12 cells but promotes these processes in Huh7 cells. Notably, co-overexpression (OE) of ZNF143 and c-Myc in AML12 cells inhibited proliferation and cell cycle progression, suggesting that ZNF143 exerts a dominant regulatory effect over c-Myc in normal hepatocytes. This study establishes a critical foundation for investigating the role of ZNF143 in hepatocyte proliferation in vivo, with potential implications for liver regeneration and transplantation therapies.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149100332","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}

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AMPK-Mediated Lipid Metabolic Reprogramming in Cancer: From Mechanisms to Targeted Therapies 肿瘤中ampk介导的脂质代谢重编程：从机制到靶向治疗

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-06 DOI: 10.1002/cbf.70314

Yuying Chen, Wen Liu, Bing Luo

{"title":"AMPK-Mediated Lipid Metabolic Reprogramming in Cancer: From Mechanisms to Targeted Therapies","authors":"Yuying Chen, Wen Liu, Bing Luo","doi":"10.1002/cbf.70314","DOIUrl":"https://doi.org/10.1002/cbf.70314","url":null,"abstract":"AMP-activated protein kinase (AMPK), a key regulator of cellular energy metabolism, is activated under conditions of energy stress to restore metabolic homeostasis by promoting catabolic pathways and inhibiting anabolic processes such as lipid synthesis. Multiple key molecules involved in lipid metabolism are regulated by AMPK, and its role in cancer progression through lipid metabolism is dual-edged. On the one hand, AMPK suppresses lipogenesis by inhibiting key regulators such as SREBP, ACC, and HMGCR, thereby limiting the biosynthetic substrates and membrane lipid availability required for tumor cell proliferation. On the other hand, AMPK activation may also enhance fatty acid oxidation and metabolic adaptation, which can support growth and survival under nutrient limitation, hypoxia, or therapeutic stress. This dual role presents therapeutic challenges but also creates opportunities for context-specific intervention. In this review, we summarize the mechanisms by which AMPK regulates lipid metabolism in cancer and discuss the current progress, therapeutic potential, and limitations of AMPK-modulating strategies.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70314","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099933","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

Capybara Oil-Based Nanoemulsion Attenuates Obesity-Induced Renal Injury Through Modulation of Inflammation, Oxidative Stress, and Fibrosis in Mice 水豚油基纳米乳通过调节小鼠炎症、氧化应激和纤维化减轻肥胖诱导的肾损伤

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-05 DOI: 10.1002/cbf.70316

Priscila G. Pereira, Luciana L. Alves, Bianca T. Ciambarella, Stela R. Ferrarini, Ana Lúcia R. Nascimento, Cherley B. V. Andrade, Alan Cesar N. Moraes, Andressa Bernardi, Fernanda V. Guimarães, Miguel P. Campos, Denia M. S. Valladão, Letícia Cruz, Jemima F. R. da Silva, Kíssila Rabelo, Jorge J. de Carvalho

{"title":"Capybara Oil-Based Nanoemulsion Attenuates Obesity-Induced Renal Injury Through Modulation of Inflammation, Oxidative Stress, and Fibrosis in Mice","authors":"Priscila G. Pereira, Luciana L. Alves, Bianca T. Ciambarella, Stela R. Ferrarini, Ana Lúcia R. Nascimento, Cherley B. V. Andrade, Alan Cesar N. Moraes, Andressa Bernardi, Fernanda V. Guimarães, Miguel P. Campos, Denia M. S. Valladão, Letícia Cruz, Jemima F. R. da Silva, Kíssila Rabelo, Jorge J. de Carvalho","doi":"10.1002/cbf.70316","DOIUrl":"https://doi.org/10.1002/cbf.70316","url":null,"abstract":"Obesity is a multifactorial disorder associated with systemic metabolic alterations and increased risk of renal injury, largely driven by chronic inflammation and oxidative stress. Bioactive lipids, particularly polyunsaturated fatty acids, have been shown to exert protective effects; however, their instability and susceptibility to oxidation may limit their therapeutic potential. In this study, we investigated the effects of a capybara oil-based nanoemulsion (NE-CO) on renal dysfunction in a mouse model of obesity. Male mice were subjected to diet-induced obesity and treated with NE-CO (100 mg/kg/day) for 4 weeks. Metabolic parameters, systolic blood pressure, urinary biomarkers, and renal morphology were evaluated. In addition, markers of inflammation, oxidative stress, and fibrosis were assessed to elucidate potential mechanisms. NE-CO treatment significantly reduced body mass and systolic blood pressure, while improving renal function, as evidenced by decreased proteinuria and normalization of urinary creatinine levels. Histological and ultrastructural analyzes revealed marked improvements in renal cortical organization. These effects were accompanied by reduced expression of pro-inflammatory markers, enhanced antioxidant defenses, and attenuation of fibrotic remodeling. Collectively, these findings demonstrate that NE-CO mitigates obesity-induced renal injury, at least in part, through modulation of inflammatory, oxidative, and fibrotic pathways. This study highlights the therapeutic potential of bioactive lipid delivery systems in the context of metabolic and renal disorders.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099820","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}

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Cell Biochemistry and Function is Advancing Our Founding Mission and Transitioning to Full Open Access 细胞生物化学和功能正在推进我们的创始使命和过渡到完全开放获取

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-05 DOI: 10.1002/cbf.70310

Robert J. W. Heath, Raphael Gaudin

引用次数: 0

PDE4DIP/Myomegalin as a Golgi-Centrosome Scaffold in Compartmentalized Signaling, Microtubule Organization, and Disease-Associated Pathway Remodeling. PDE4DIP/ myomegin在区隔化信号、微管组织和疾病相关通路重构中的作用

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-01 DOI: 10.1002/cbf.70325

Cong Wang, Chunjing Bian, Zhe Wang, Tao Luo

{"title":"PDE4DIP/Myomegalin as a Golgi-Centrosome Scaffold in Compartmentalized Signaling, Microtubule Organization, and Disease-Associated Pathway Remodeling.","authors":"Cong Wang, Chunjing Bian, Zhe Wang, Tao Luo","doi":"10.1002/cbf.70325","DOIUrl":"https://doi.org/10.1002/cbf.70325","url":null,"abstract":"PDE4DIP/Myomegalin was originally identified as a Golgi- and centrosome-associated protein that interacts with phosphodiesterase 4D, but subsequent work has placed it within a broader network of organelle-associated signaling and cytoskeletal regulation. This review examines PDE4DIP/Myomegalin as a coiled-coil-rich scaffold linking compartmentalized cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling, Golgi-centrosome organization, microtubule architecture, and disease-associated pathway remodeling. At the centrosome, long PDE4D-binding myomegalin forms retain PDE4D3 and restrict local PKA activity, thereby influencing Hedgehog signaling. At the Golgi, AKAP9/AKAP450 provides a major scaffold, while selected myomegalin forms support Golgi-derived microtubule organization and endoplasmic reticulum-Golgi trafficking. In KRAS-mutant colorectal cancer models, PDE4DIP promotes tumor growth and MEK inhibitor resistance through Golgi-associated NF1/RAS pathway remodeling. In non-small cell lung cancer, PDE4DIP cooperates with AKAP9 to maintain Golgi localization and stability of PKA regulatory subunit II alpha; PDE4DIP loss activates PKA/cAMP response element-binding protein signaling and suppresses tumor growth. Cardiovascular studies link myomegalin isoform 4 to sarcomeric PKA signaling, co-occurring PDE4DIP and DES variants to conduction phenotypes, and PDE4DIP dysregulation to left ventricular noncompaction-associated cellular changes, although the evidence remains context dependent. Neurological and retinal disease associations remain largely exploratory. Recent work links a PDE4DIP-AKAP9 interaction to cytoskeletal integrity and RAS-ERK/AKT signaling in podocyte injury. Overall, PDE4DIP/Myomegalin is best understood as an organelle-associated organizer whose effects depend on the experimentally reported form, binding partners, and subcellular address rather than on a single linear pathway.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":"e70325"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Patient-Derived Organoids in Functional Precision Oncology: Tumor Modeling, Drug-Response Prediction, and Clinical Translation. 功能精准肿瘤学中患者来源的类器官：肿瘤建模、药物反应预测和临床翻译。

IF 3.5 3区生物学

Cell Biochemistry and Function Pub Date : 2026-10-01 DOI: 10.1002/cbf.70321

Abdullah Jabri, Mohamed Alsharif, Abdulaziz Mhannayeh, Bader Taftafa, Dania Sibai, Abdulrahman Elsalti, Raghad Alsharif, Tanveer Ahmad Mir, Mohammed Imran Khan, Jahan Salma, Ahmed Yaqinuddin

{"title":"Patient-Derived Organoids in Functional Precision Oncology: Tumor Modeling, Drug-Response Prediction, and Clinical Translation.","authors":"Abdullah Jabri, Mohamed Alsharif, Abdulaziz Mhannayeh, Bader Taftafa, Dania Sibai, Abdulrahman Elsalti, Raghad Alsharif, Tanveer Ahmad Mir, Mohammed Imran Khan, Jahan Salma, Ahmed Yaqinuddin","doi":"10.1002/cbf.70321","DOIUrl":"https://doi.org/10.1002/cbf.70321","url":null,"abstract":"Patient-derived organoids (PDOs) have emerged as an effective experimental platform for bridging the long-standing gap between traditional in vitro cancer models and the biological complexity of actual tumors. These three-dimensional cultures (3D), derived directly from patient tissues, preserve essential architectural, genomic, and phenotypic characteristics of their tumors of origin, enabling more accurate modeling of tumor heterogeneity and disease evolution. Over the last decade, rapid methodological advances in organoid culture systems, extracellular matrices (ECMs), and growth factor optimization have facilitated the establishment of organoid models for a wide range of malignancies and the development of large living biobanks representing diverse patient populations. These models are increasingly being utilized to study cancer biology, elucidate mechanisms of treatment resistance, and evaluate patient-specific therapeutic responses, highlighting their potential as tools for precision oncology. However, important challenges remain, including incomplete representation of the tumor microenvironment (TME), variability in culture conditions, and limited scalability, and the need for greater standardization and validation. Consequently, although PDOs show considerable promise for translational research and personalized medicine, their routine clinical implementation remains largely investigational, and their clinical utility has not yet been fully established. This review examines the technological foundations of PDO generation, assesses their role as experimental models of tumor biology, and discusses their expanding applications in translational cancer research and precision oncology while highlighting key challenges that must be addressed before their widespread clinical adoption.","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 10","pages":"e70321"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0