Frontiers in Cell and Developmental Biology最新文献

{"title":"Biogenesis and homeostasis of mast cell lysosome related secretory granules.","authors":"Ronit Sagi-Eisenberg","doi":"10.3389/fcell.2025.1603999","DOIUrl":"10.3389/fcell.2025.1603999","url":null,"abstract":"<p><p>Mast cells (MCs) are sentinel cells of the immune system that play important protective roles in innate host defenses but are also key effectors of allergic responses and chronic inflammatory diseases. Both physiological and pathophysiological responses of MCs are mediated by the release of inflammatory mediators, many of which are stored, preformed, in secretory granules (SGs), and released by regulated exocytosis in response to multiple stimuli. MC SGs belong to the family of lysosome related organelles (LROs), as indicated by their content of lysosomal hydrolases, lysosomal membrane proteins and acidic pH. The SGs derive from the Golgi and increase in size in a quantal manner by their fusion with additional SGs. They have access to external cargo, which they acquire by fusion with endosomes and contain LC3, which they acquire by fusion with amphisomes. This review discusses the underlying mechanisms of MC SG biogenesis and remodeling.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1603999"},"PeriodicalIF":4.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atypical Hippo signaling network: uncovering novel insights into head and neck cancer biology and advancements in precision intervention.","authors":"Pengfei Yang, Shujuan Li","doi":"10.3389/fcell.2025.1610471","DOIUrl":"10.3389/fcell.2025.1610471","url":null,"abstract":"<p><p>As a major global health challenge with rising incidence and poor prognosis, head and continues to impose a significant clinical burden due to its aggressive biological behavior and frequent therapeutic resistance. Within this context, the atypical Hippo signaling pathway emerges as a crucial regulatory network, integrating diverse components including core kinases (TAO kinases, MAP4K family, NDR1/2 kinases), cell polarity determinants (CRUMBS, SCRIBBLE), junctional adhesion molecules (AMOT family), phosphorylation mediators (14-3-3 proteins), and tumor suppressors (NF2, RASSF family). This multifaceted system governs fundamental cellular processes spanning proliferation, apoptosis, migratory capacity, and immune microenvironment modulation. Notably, post-translational modifications (ubiquitination, acetylation, SUMOylation) of pathway components dynamically regulate the stability and activity of downstream effectors YAP/TAZ, whose sustained activation through molecular aberrations drives tumor progression and treatment resistance in head and neck malignancies.The pathway's extensive crosstalk with Wnt signaling, NF-κB cascades, and estrogen receptor networks creates context-dependent regulatory plasticity that contributes to tumor heterogeneity. Current therapeutic innovation focuses on molecular diagnostics and precision targeting approaches, including direct YAP/TAZ-TEAD complex inhibitors, upstream receptor modulators, and rational combinations with immune checkpoint blockade. Future investigations should employ multi-omics profiling to delineate tumor subtype-specific regulatory architectures while advancing novel drug delivery platforms. These efforts promise to translate mechanistic insights into multi-targeted therapeutic strategies capable of overcoming resistance mechanisms and improving survival outcomes for this therapeutically challenging malignancy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1610471"},"PeriodicalIF":4.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A dual inhibitor of TrxR1 and XIAP induces pyroptosis in melanoma.","authors":"Yuan Wang, Xiangmei Li, Xinyue Dong, Haokun Yuan, Ruiqin Fang, Ran Zhang, Wei-Jia Wang","doi":"10.3389/fcell.2025.1542356","DOIUrl":"10.3389/fcell.2025.1542356","url":null,"abstract":"<p><p>Malignant melanoma ranks among the most aggressive forms of cancer, with high rates of metastasis and recurrence, as well as a poor prognosis. Consequently, an urgent need is to develop novel precision therapeutic strategies and corresponding drugs. Previous studies have shown that both X-linked inhibitor of apoptosis (XIAP) and thioredoxin reductase 1 (TrxR1) participate in the resistance of melanoma to chemotherapy-induced cell death. In this study, we designed and synthesized a series of derivatives of natural compounds derived from <i>Toona sinensis</i> to simultaneously inhibit TrxR1 activity and destabilize the XIAP protein. The new dual-target inhibitor TRI-03 has significant antiproliferative effects on melanoma cells. Mechanistically, TRI-03 not only increases intracellular reactive oxygen species (ROS) levels by inhibiting TrxR1 activity but also decreases XIAP expression, leading to the activation of the caspase-9/caspase-3/GSDME axis and irreversible GSDME-mediated pyroptosis in melanoma cells. Our <i>in vivo</i> animal study confirmed that TRI-03 effectively inhibits melanoma proliferation and metastasis without severe side effects. Therefore, our study identified TRI-03 as a potential antitumor candidate for future development to address melanoma.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1542356"},"PeriodicalIF":4.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SNHG12 downregulation induces follicular dysplasia by modulating the glycolysis of granulosa cell in polycystic ovary syndrome.","authors":"Sisi Yan, Bing Qu, Yu Chen, Qiuji Wu, Jinli Ding, Hui Qiu","doi":"10.3389/fcell.2025.1585987","DOIUrl":"10.3389/fcell.2025.1585987","url":null,"abstract":"<p><strong>Introduction: </strong>Polycystic ovary syndrome (PCOS) is characterized by follicular dysplasia, with granulosa cells (GCs) glycolysis playing a pivotal role in this pathology. Although the involvement of long noncoding RNAs (lncRNAs) in diverse biological processes of PCOS has been well documented, the molecular mechanism of lncRNA small nucleolar RNA host gene 12 (SNHG12) in PCOS remains unclear.</p><p><strong>Methods: </strong>In this study, we measured SNHG12 expression in GCs of PCOS patients and healthy controls using RT-PCR and performed correlation analysis between SNHG12 expression and glycolytic markers. Using granulosa-like tumor (KGN) cells, we investigated glycolytic capacity and examined the relationship among SNHG12, PTEN and HMGB1 through RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays. Finally, DHEA-induced PCOS mice was constructed using SNHG12 adenovirus to explore its role in PCOS.</p><p><strong>Results: </strong>SNHG12 expression was significantly downregulated in GCs from PCOS patients compared with healthy controls, and showed positive correlation with glycolytic markers. Functional studies demonstrated that SNHG12 knockdown impaired glycolysis in KGN cells, while SNHG12 overexpression partially restored glycolysis. Furthermore, SNHG12-induced glycolysis affected apoptosis of KGN cells, which mediated follicular dysplasia through lactate production and apoptotic pathways. <i>In vivo</i>, adenovirus-mediated SNHG12 overexpression alleviated the symptoms of PCOS mice. Mechanistically, RIP and ChIP assays revealed that SNHG12 interacts with HMGB1 and inhibits PTEN transcription by preventing HMGB1 from binding to the PTEN promoter, thereby promoting glycolysis in KGN cells.</p><p><strong>Conclusion: </strong>Our findings collectively demonstrate that the SNHG12/HMGB1/PTEN axis serves as a novel regulatory mechanism in PCOS by modulating glycolytic-mediated follicular dysplasia in GCs, offering a potential therapeutic target for PCOS.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1585987"},"PeriodicalIF":4.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Large language model-based multimodal system for detecting and grading ocular surface diseases from smartphone images.","authors":"Zhongwen Li, Zhouqian Wang, Liheng Xiu, Pengyao Zhang, Wenfang Wang, Yangyang Wang, Gang Chen, Weihua Yang, Wei Chen","doi":"10.3389/fcell.2025.1600202","DOIUrl":"10.3389/fcell.2025.1600202","url":null,"abstract":"<p><strong>Background: </strong>The development of medical artificial intelligence (AI) models is primarily driven by the need to address healthcare resource scarcity, particularly in underserved regions. Proposing an affordable, accessible, interpretable, and automated AI system for non-clinical settings is crucial to expanding access to quality healthcare.</p><p><strong>Methods: </strong>This cross-sectional study developed the Multimodal Ocular Surface Assessment and Interpretation Copilot (MOSAIC) using three multimodal large language models: gpt-4-turbo, claude-3-opus, and gemini-1.5-pro-latest, for detecting three ocular surface diseases (OSDs) and grading keratitis and pterygium. A total of 375 smartphone-captured ocular surface images collected from 290 eyes were utilized to validate MOSAIC. The performance of MOSAIC was evaluated in both zero-shot and few-shot settings, with tasks including image quality control, OSD detection, analysis of the severity of keratitis, and pterygium grading. The interpretability of the system was also evaluated.</p><p><strong>Results: </strong>MOSAIC achieved 95.00% accuracy in image quality control, 86.96% in OSD detection, 88.33% in distinguishing mild from severe keratitis, and 66.67% in determining pterygium grades with five-shot settings. The performance significantly improved with the increasing learning shots (p < 0.01). The system attained high ROUGE-L F1 scores of 0.70-0.78, depicting its interpretable image comprehension capability.</p><p><strong>Conclusion: </strong>MOSAIC exhibited exceptional few-shot learning capabilities, achieving high accuracy in OSD management with minimal training examples. This system has significant potential for smartphone integration to enhance the accessibility and effectiveness of OSD detection and grading in resource-limited settings.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1600202"},"PeriodicalIF":4.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"snRNA-seq reveals subcutaneous white adipose tissue remodeling upon return to thermoneutrality after cold stimulation.","authors":"Yusha Yang, Guanyu Zhang, Ting Yi, Shuran Yang, Shuai Wu, Yongqiang Zhang, Li Zhang, Xi Li, Xiuxuan Wu, Jun Li, Danfeng Yang","doi":"10.3389/fcell.2025.1578180","DOIUrl":"10.3389/fcell.2025.1578180","url":null,"abstract":"<p><strong>Introduction: </strong>Cold stimulation induces browning of subcutaneous white adipose tissue (sWAT), making it a prime target for treating obesity and metabolic disorders. However, this remodeling is reversible: upon return to thermoneutrality (rewarming), sWAT whitens and loses its enhanced metabolic functions. Given the limited understanding of the microscopic dynamic changes and underlying mechanisms during this process, we established a temporally dynamic mouse model spanning the entire period from cold stimulation to the return to thermoneutrality, with inguinal sWAT (iWAT) selected as the study subject.</p><p><strong>Methods: </strong>Based on preliminary data demonstrating stabilization in iWAT histology, expression levels of key thermogenic proteins, and the bulk transcriptome, we selected the two-week time point after the return to thermoneutrality for detailed analysis. Subsequently, we employed single-nucleus RNA sequencing (snRNA-seq) to comprehensively characterize iWAT cellular dynamics during cold stimulation and the subsequent two-week period after the return to thermoneutrality.</p><p><strong>Results: </strong>Our findings revealed that while iWAT phenotypically reverts to a white state after 2 weeks of rewarming, as evidenced by structural, functional, and bulk transcriptomic characteristics, significant cold-induced molecular and cellular signatures persist. Specifically, we observed altered differentiation trajectories in both adipose stem and progenitor cells (ASPCs) and adipocytes, suggesting dedifferentiation and reprogramming tendencies. Furthermore, the ANGPTL signaling pathway, activated in thermogenic adipocyte subpopulation A3 during cold stimulation, remained active and influenced cell-cell communication even after the loss of thermogenic capacity.</p><p><strong>Discussion: </strong>hese findings provide novel insights into elucidating the complex cellular and molecular mechanisms underlying the temperature-dependent plasticity of iWAT, and suggest that the ANGPTL signaling pathway may play a potential role in maintaining the white phenotype of iWAT after withdrawal from cold stimulation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1578180"},"PeriodicalIF":4.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12138199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary modifications affect renal recovery during the healing phase following ischemic acute ischemic kidney injury.","authors":"Junseok Jeon, Kyungho Lee, Hojin Jeon, Kyeong Eun Yang, Cheol-Jung Lee, Jung Eun Lee, Ghee Young Kwon, Wooseong Huh, Hye Ryoun Jang","doi":"10.3389/fcell.2025.1494660","DOIUrl":"10.3389/fcell.2025.1494660","url":null,"abstract":"<p><strong>Introduction: </strong>The effects of dietary modifications, such as varying amounts of salt, fat, and protein intake on the healing phase of acute kidney injury (AKI) remain to be elucidated. We investigated the effects of low- or high-salt/fat/protein diets on the intrarenal immunologic micromilieu and healing after renal ischemia-reperfusion injury (IRI) using murine ischemic AKI and human kidney-2 (HK-2) cell hypoxia models.</p><p><strong>Methods: </strong>Three cohorts of male C57BL/6 mice (9-weeks old) were fed the designated diet from the third day following renal IRI until sacrifice (6 or 12 weeks after bilateral or unilateral IRI, respectively) in groups as follows: cohort 1, control, high- and low-salt/fat/protein; cohort 2, control, high- and low-salt; cohort 3, control, high- and low-fat/protein. Hypoxic HK-2 cells were treated with sodium chloride, amino acids, or fatty acids.</p><p><strong>Results: </strong>Low-salt/fat/protein diet aggravated interstitial fibrosis, enhanced TGF-β expression, and induced more proinflammatory changes after bilateral IRI. High-salt diet aggravated renal tubular damage and enhanced the expression of intrarenal TGF-β after bilateral IRI, whereas low-salt diet enhanced the expression of intrarenal TGF-β after unilateral IRI. Low-salt diet induced more proinflammatory changes after bilateral IRI. Blood urea nitrogen levels were lower in the low fat/protein group than that in the control group following IRI. However, low-fat/protein diet aggravated interstitial fibrosis and enhanced intrarenal TGF-β expression after unilateral IRI. High sodium- or protein-containing media suppressed the proliferation of hypoxic HK-2 cells, whereas high lipid-containing media enhanced the proliferation of hypoxic HK-2 cells.</p><p><strong>Conclusion: </strong>Excessive low or high salt, low fat, and low protein diet may adversely affect the healing process following renal IRI, supporting the importance of adequate and balanced nutrition during the recovery phase of ischemic AKI.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1494660"},"PeriodicalIF":4.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integration of machine learning and bulk sequencing revealed exosome-related gene FOSB was involved in the progression of abdominal aortic aneurysm.","authors":"Xianlu Ma, Hongjie Zhou, Ren Wang","doi":"10.3389/fcell.2025.1554972","DOIUrl":"10.3389/fcell.2025.1554972","url":null,"abstract":"<p><strong>Background: </strong>Abdominal aortic aneurysm (AAA), characterized by the pathological dilation of the abdominal aorta, was associated with immune response and inflammation. However, the key genes involved in the occurrence and progression of AAA remains unclear.</p><p><strong>Methods: </strong>We applied Weighted Gene Co-expression Network Analysis (WGCNA) and Support Vector Machine Recursive Feature Elimination (SVM-RFE) to screen for significant genes from the Gene Expression Omnibus (GEO) dataset. The CIBERSORT algorithm was utilized to analyze the correlation between these genes and immune cell infiltration. Additionally, we validated the expression of FosB proto-oncogene, AP-1 transcription factor subunit (FOSB) in a murine model of AAA. FOSB was overexpressed and knocked out in vascular smooth muscle cells (VSMCs). Cell viability and apoptosis were assessed using the CCK-8 assay and flow cytometry, respectively. The levels of MMP2 and MMP9 in the cell supernatants were quantified by ELISA. The expression of contraction-related markers α-SMA and SM22α, and the synthetic marker OPN, was analyzed by qRT-PCR and Western blot.</p><p><strong>Results: </strong>A total of 44 differentially expressed genes were identified, revealing distinct expression patterns between AAA and normal samples. WGCNA identified two key gene modules that were strongly correlated with immune and inflammatory responses, with the hub genes from these modules enriched in immune-related pathways. FOSB was positively correlated with monocytes, plasma cells, eosinophils, and T follicular helper cells. It was further validated in an AngII-induced AAA mouse model. Overexpression of FOSB significantly increased the expression levels of MMP2 and MMP9 in VSMCs. Additionally, FOSB overexpression inhibited the expression of contractile phenotype markers α-SMA and SM22α, while promoting the expression of synthetic phenotype marker OPN.</p><p><strong>Conclusion: </strong>Exosome-related gene FOSB was involved in the progression of abdominal aortic aneurysm. FOSB represents a promising potential therapeutic target for mitigating the progression of Abdominal Aortic Aneurysm.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1554972"},"PeriodicalIF":4.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12142044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-driven prediction of cycloplegic refractive error in Chinese children.","authors":"Bichi Chen, Li Tian, Fuyue Tian, Qiaochu Yang, Ying Ruan, Ying Li, Min Cao, Chuanyan Wu, Maoyuan Yang, Suzhong Xu, Ruzhi Deng","doi":"10.3389/fcell.2025.1608494","DOIUrl":"10.3389/fcell.2025.1608494","url":null,"abstract":"<p><strong>Objective: </strong>To develop and validate machine learning (ML) models for predicting cycloplegic spherical equivalent refraction (SER) using non-cycloplegic parameters, addressing challenges in pediatric ophthalmic assessments.</p><p><strong>Methods: </strong>A prospective cohort of 2,274 Chinese children (4,548 eyes) aged 3∼16 years was stratified into development (<i>n</i> = 1819) and validation (<i>n</i> = 455) datasets. Six ML models (linear regression, random forest, extreme gradient boosting, multilayer perceptron, support vector machine, and light gradient boosting machine) were trained on demographics, non-cycloplegic refractive error, and ocular biometrics. Model performance was evaluated using <i>R</i> ^<i>2</i> , mean error (ME), mean absolute error (MAE), and clinical accuracy (proportions within ±0.50 D/±1.00 D).</p><p><strong>Results: </strong>In the validation dataset, ML models predicted cycloplegic SER with high <i>R</i> ^<i>2</i> (0.920∼0.934), low ME (-0.004∼0.015 D) and MAE (0.385∼0.413 D). The multilayer perceptron model achieved the highest accuracy (<i>R</i> ^<i>2</i> = 0.934, MAE = 0.385 D), with 73.08% and 94.29% of predictions within ±0.50 D and ±1.00 D, respectively. Performance was optimal in children aged 7∼10 years (77.17∼79.70% within ±0.50 D) and those with low myopia (-3.00 to -0.50 D; 83.09∼83.56% within ±0.50 D). Non-cycloplegic measurements systematically overestimated myopia (mean difference: -0.39 ± 0.71 D, <i>P</i> < 0.001), particularly in younger children and hyperopic eyes.</p><p><strong>Conclusion: </strong>ML models provide accurate estimates of cycloplegic SER using non-cycloplegic parameters, offering a practical alternative for pediatric refractive assessments when cycloplegia is infeasible.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1608494"},"PeriodicalIF":4.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organoids technology in cancer research: from basic applications to advanced <i>ex vivo</i> models.","authors":"Luca Varinelli, Oscar Illescas, Ewelina Julia Lorenc, Davide Battistessa, Marzia Di Bella, Susanna Zanutto, Manuela Gariboldi","doi":"10.3389/fcell.2025.1569337","DOIUrl":"10.3389/fcell.2025.1569337","url":null,"abstract":"<p><p>Patient-derived organoids (PDOs) are tridimensional cultures derived from the stem component of a tissue. They preserve the genetic and phenotypic characteristics of the tissue of origin, and represent valuable <i>in vitro</i> models for drug screening, biomarker discovery, cell therapy and genetic modification. Importantly, PDOs reproduce the tumor behavior and can predict therapeutic responses, making them relevant for clinical applications for personalized therapies. PDOs may also be used for studying the interactions between cancer cells and the tumor microenvironment (TME). These interactions are driven by biochemical factors released by the cells, and biomechanical events such as the remodeling of the extracellular matrix (ECM). In recent years, it has become evident that the interactions between cancer cells and the TME have an impact on tumor development and on the efficacy of cancer therapy Therefore, targeting both tumor cells and the TME may improve patient response to treatment. Most PDO culture protocols are limited to epithelial cells. However, recent advances such as use of decellularized ECM (dECM) scaffolds have allowed for the development of <i>in vivo</i>-like environments that host diverse cell types, both normal and pathological, in a tridimensional (3D) manner that closely mimics the complexity of the TME. dECM-based models effectively replicate the interactions between tumor cells, ECM and the microenvironment, are easy to analyze and adaptable for drug testing. By incorporating TME components and therapeutic agents, these models offer an advanced platform for preclinical testing.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1569337"},"PeriodicalIF":4.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}