Experimental cell research最新文献

{"title":"Single cell RNA sequencing reveals shifts in cell maturity and function of endogenous and infiltrating cell types in response to acute intervertebral disc injury.","authors":"Sade W Clayton, Aimy Sebastian, Stephen P Wilson, Nicholas R Hum, Remy E Walk, Garrett W D Easson, Rachana Vaidya, Kaitlyn S Broz, Gabriela G Loots, Simon Y Tang","doi":"10.1016/j.yexcr.2025.114691","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114691","url":null,"abstract":"<p><p>Intervertebral disc (IVD) degeneration contributes to disabling back pain. Degeneration can be initiated by injury and progressively leads to an irreversible loss of cells and function. IVD function restoration through cell replacement therapies have had limited success due to knowledge gaps in the critical cell populations important for repair. Here, we used single cell RNA sequencing to identify the transcriptional changes of IVD resident and infiltrating cell populations from Control and Injured coccygeal IVDs extracted from 12-week-old female C57BL/6J mice 7 days post injury. Clustering, gene ontology, and pseudotime trajectory analyses determined transcriptomic divergences with injury, flow cytometry identified they types of infiltrating immune cells, and immunofluorescence was utilized to define mesenchymal stem cell (MSC) localization. We identified 11 distinct clusters that included IVD, immune, vascular cells, and MSCs. Differential gene expression analysis determined that Outer Annulus Fibrosus, Neutrophils, Saa2-High MSCs, Macrophages, and Krt18⁺ Nucleus Pulposus (NP) cells were the major drivers of transcriptomic differences between Control and Injured cells. Gene ontology revealed that the most upregulated biological pathways were angiogenesis and T cell-related while wound healing and ECM regulation were downregulated. Pseudotime trajectory analyses revealed that IVD injury directed cells towards increased differentiation in all clusters, except for Krt18⁺ NP cells which remained in a less mature cell state. Saa2-High and Grem1-High MSCs populations shifted towards more differentiated IVD cells profiles with injury and localized distinctly within the IVD. This study revealed novel MSC populations with the potential to be leveraged for future IVD repair studies.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114691"},"PeriodicalIF":3.5,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764800","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}

{"title":"Understanding Variability in Cell Death Modes and Sensitivity: Potential Implications for Targeted Cancer Therapies.","authors":"Magdalena Węgrzyn, Malgorzata Adamiec-Organisciok, Anahit Dawicka, Daniel Fochtman, Seweryn Galecki, Ngoni Magate, Kinga Bartel, Daria Gendosz de Carillo, Emilia Witek-Zelazny, Magdalena Skonieczna","doi":"10.1016/j.yexcr.2025.114688","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114688","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114688"},"PeriodicalIF":3.5,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764801","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}

{"title":"Tumor suppressor OSR1 is modified by SUMO1 and regulates the Wnt/β-catenin signaling pathway in HCC.","authors":"Xinju Lin, Yuming Liu, Zisen Lai, Xiaopei Wang, Yongliang Cui, Shangeng Weng","doi":"10.1016/j.yexcr.2025.114693","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114693","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the deadliest cancers in the world. Exploring the underlying molecular mechanisms of HCC, such as those involving small ubiquitin-related modifier (SUMO) and its targets, is worthwhile. A total of 12 HCC tissue samples were collected for immunohistochemistry. The interaction between SUMO1 and OSR1 was confirmed by co-IP and immunofluorescence (IF). The expression (qPCR and western blot), cytological function (CCK-8, clone formation and transwell assays) of OSR1 was further investigated in HepG2 cells. The anti-tumor function of OSR1 was also verified in the nude mouse xenograft model. Western blot analysis revealed the underlying downstream signaling pathway of SUMO1-modified OSR1 in HCC. Up-regulated co-expression of SUMO1-OSR1 was observed in the HepG2 cells. Through the cytological experiments and a nude mouse xenograft model, we found that OSR1 is a tumor suppressor gene that inhibits the proliferation and invasion of the HepG2 cells in vitro. Intriguingly, SUMO1-OE antagonized OSR1-mediated β-catenin regulation: in nuclei, SUMO1-OE enhanced β-catenin expression, counteracting OSR1-OE-induced suppression, whereas in the cytoplasm, SUMO1-OE inhibited β-catenin accumulation and attenuated OSR1-OE-driven promotion. Hypoxia reversed these effects, suggesting an oxygen-sensitive interplay between SUMO1 and OSR1. In conclusion, OSR1 is a tumor suppressor in HCC via attenuation of the Wnt/β-catenin pathway. SUMO1 modifies OSR1, suppressing the Wnt/β-catenin signaling pathway and promoting the occurrence and development of HCC; this effect of which could be enhanced by hypoxia.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114693"},"PeriodicalIF":3.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759585","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}

{"title":"The RNA-binding protein HuR regulates microRNA biogenesis via increased Drosha expression.","authors":"Lin Liu, Linxiao Wang, Yanjun Wang, Ran Zhuang, Yuan Zhang, Junjie Li, Jiangang Xie, Wen Yin","doi":"10.1016/j.yexcr.2025.114686","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114686","url":null,"abstract":"<p><strong>Background: </strong>The biogenesis of microRNAs (miRNAs) undergoes substantial alterations in response to various stressors. Drosha, a pivotal regulator of miRNA biogenesis, plays a critical role in cellular responses to external stimuli. The RNA-binding protein HuR is upregulated upon cellular stress. However, under severe or prolonged stress conditions, HuR levels may decline, impairing its protective functions.</p><p><strong>Methods: </strong>To investigate the influence of HuR on miRNA expression, miRNA sequencing was employed to profile expression in IEC-6 intestinal epithelial cells following HuR silencing. Additionally, the effect of HuR overexpression on Drosha expression and activity was assessed. Bioinformatics analyses, biochemical assays, and molecular biology techniques were utilized to elucidate the mechanisms by which HuR interacts with Drosha mRNA, modulating both its translation and transcription.</p><p><strong>Results: </strong>HuR silencing resulted in a significant downregulation of nearly all miRNAs, with no observed impact on piRNA biogenesis. Conversely, HuR overexpression led to increased Drosha expression, regulated through HuR's direct binding to the 3'-UTR of Drosha mRNA. Moreover, HuR indirectly promoted Drosha transcription by elevating c-Myc levels. In a mouse model of thoracic trauma, diminished HuR expression in the intestinal epithelium correlated with reduced Drosha levels, impairing miRNA biogenesis and enhancing apoptosis.</p><p><strong>Conclusions: </strong>These findings underscore the essential role of HuR in the regulation of miRNA biogenesis through Drosha, with implications for stress responses and intestinal injury. The HuR-Drosha axis emerges as a promising therapeutic target for modulating miRNA biogenesis.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114686"},"PeriodicalIF":3.3,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717831","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}

{"title":"Chimeric antigen receptor (CAR)-NK cell therapy in gastrointestinal (GI) cancers; a new arena","authors":"Ali G. Alkhathami ,&nbsp;Abdulrahman T. Ahmed ,&nbsp;Ahmed Hussn ,&nbsp;S. RenukaJyothi. ,&nbsp;Rajashree Panigrahi ,&nbsp;Hussein Riyadh Abdul Kareem Al-Hetty ,&nbsp;Hansi Negi ,&nbsp;Pushkar Jassal ,&nbsp;Fathi Jihad Hammady ,&nbsp;Salah Abdulhadi Salih","doi":"10.1016/j.yexcr.2025.114683","DOIUrl":"10.1016/j.yexcr.2025.114683","url":null,"abstract":"<div><div>Tumor microenvironment (TME) is highly complex, and immune escape is a crucial characteristic of malignancies that promotes tumor development and spread. According to studies, the limited success achieved by T cell immunotherapy highlights the growing importance of other advanced immunotherapies, specifically those based on natural killer (NK) cells. Human NK cells are the primary innate immune cells that combat malignancies and exhibit significant diversity within the TME of gastrointestinal (GI) cancers. There is currently a growing interest in the advancement of chimeric antigen receptor (CAR)-engineered NK cells for GI cancer immunotherapy. The advantages of CAR-NK cells over CAR-T cells include enhanced safety, with minimal or no occurrence of cytokine release syndrome (CRS) and graft-versus-host disease (GVHD). Additionally, CAR-NK cells employ many methods to stimulate cytotoxic function and are very feasible for \"off-the-shelf\" manufacture. These effector cells can be genetically altered to specifically recognize different antigens, enhance their ability to multiply and survive in the body, increase their ability to enter GI cancers and overcome resistance in the tumor microenvironment. This ultimately leads to a desired anti-tumor response. Significantly, CAR-NK cells serve as antigen receptors for tumor-associated antigens (TAAs), effectively diverting NK cells and promoting tumor-related immunosurveillance. This study examines the advancements in the therapeutic capabilities of CAR-NK cells for treating GI cancers.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114683"},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682246","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}

{"title":"Role of METTL3 in high glucose-induced trophoblast cell pyroptosis by the CEBPB/miR-96-5p/CCND2 axis via m6A modification","authors":"Yeqing Su ,&nbsp;Lulu Wang ,&nbsp;Danna He","doi":"10.1016/j.yexcr.2025.114670","DOIUrl":"10.1016/j.yexcr.2025.114670","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) is regarded as abnormally elevated glucose contents at pregnancy period. We attempt to explore the interaction of methyltransferase 3 (METTL3) in high glucose (HG)-treated trophoblast cell pyroptosis, thereby finding a new target for GDM treatment. HTR8/SVneo cells were stimulated using HG to establish GDM models for the following assessment of METTL3, CCAAT enhancer binding protein beta (CEBPB), microRNA (miR)-96-5p and cyclin D2 (CCND2). Levels of pyroptosis-related indicators were verified. m6A level in GDM and the enrichment of m6A on CEBPB were evaluated. The binding relation between CEBPB and miR-96-5p and between miR-96-5p and CCND2 were verified. Roles of METTL3 silencing, CEBPB overexpression, miR-96-5p silencing, and CCND2 overexpression in HG-induced trophoblast cell pyroptosis were detected. METTL3, CEBPB, and CCND2 were upregulated in GDM placenta tissues and HG-induced HTR8/SVneo cells, while miR-96-5p was downregulated. Levels of pyroptosis-related indicators were upregulated, which were counteracted upon METTL3 silencing. Mechanically, METTL3-mediated m6A modification promoted CEBPB expression, inhibited miR-96-5p, which targeted CCND2. CEBPB overexpression, miR-96-5p silencing, and CCND2 could neutralize the suppressive effect of METTL3 knockdown on HG-induced trophoblast cell pyroptosis. METTL3-mediated m6A modification promoted CEBPB expression to suppressmiR-96-5p expression and promote CCND2 expression, thus strengthening HG-induced trophoblast cell pyroptosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114670"},"PeriodicalIF":3.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599865","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}

{"title":"DNAJC6 in acute kidney injury: A novel target for protecting renal tubular epithelial cells through PGC-1α-mediated mitochondrial homeostasis","authors":"Liyun Ma ,&nbsp;Jialiang Hui ,&nbsp;Guangting He ,&nbsp;Zaisheng Qin","doi":"10.1016/j.yexcr.2025.114682","DOIUrl":"10.1016/j.yexcr.2025.114682","url":null,"abstract":"<div><h3>Background</h3><div>Acute kidney injury (AKI) is a severe clinical syndrome that critically threatens patients' lives and health. It is characterized by complex pathogenesis and lacks effective therapeutic strategies. Mitochondrial homeostasis disruption plays a pivotal role in AKI progression, yet its precise molecular mechanisms remain unclear. This study aimed to investigate the role of DNAJC6 in AKI and its molecular mechanism of mitochondrial homeostasis regulation.</div></div><div><h3>Methods</h3><div>Utilizing cisplatin-induced mouse AKI models and human proximal tubular epithelial cell line HK-2, we employed multiple experimental approaches including bioinformatics analysis, cell transfection, immunohistochemical staining, immunofluorescence, TUNEL assay, and mitochondrial function detection to explore the role and molecular mechanisms of DNAJC6 in AKI.</div></div><div><h3>Results</h3><div>In cisplatin-induced AKI models, renal DNAJC6 expression decreased. DNAJC6 overexpression markedly alleviated kidney injury, reduced cell apoptosis, and attenuated inflammatory responses. Mechanistic investigations revealed that DNAJC6 regulated mitochondrial homeostasis by promoting PGC-1α nuclear translocation. Specifically, DNAJC6 improved mitochondrial respiratory function and reduced mitochondrial oxidative stress levels. Moreover, DNAJC6 enhanced mitochondrial biogenesis and suppressed inflammatory factor expression. Upon PGC-1α knockdown, DNAJC6's protective effects were almost completely abolished, confirming that PGC-1α was a critical molecular mediator.</div></div><div><h3>Conclusion</h3><div>This study elucidated the molecular mechanism by which DNAJC6 protected renal tubular epithelial cells through PGC-1α-mediated mitochondrial homeostasis in AKI. These findings not only provide a novel perspective on AKI pathogenesis but also offer a crucial theoretical foundation for developing potential therapeutic strategies. DNAJC6 emerges as a promising molecular target for AKI treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114682"},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697990","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}

{"title":"Research progress of ASIC family in tumors","authors":"Xing Wan ,&nbsp;Liming Zhou","doi":"10.1016/j.yexcr.2025.114681","DOIUrl":"10.1016/j.yexcr.2025.114681","url":null,"abstract":"<div><div>As a proton-gated cation channel, the acid-sensitive ion channels (ASICs) is capable of sensing changes in the extracellular pH value. ASICs are widely distributed and apart from physiological functions, play a role in various diseases related to acidity, such as pain, inflammation, and ischemia. Moreover, studies have shown that ASICs also have an impact on the occurrence, development, invasion, metastasis, and drug resistance of tumors under acidosis conditions. Although the underlying mechanisms of ASIC-mediated processes have not been extensively explored, these studies suggest that ASICs may emerge as novel biomarkers and therapeutic targets, offering new perspectives for the development of alternative cancer therapies. This article reviews the latest progress of ASICs in tumors, summarizes the classic substances that affect their activity, and analyzes the future research directions, providing a basis for them to be potential targets for tumor treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114681"},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144679027","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}

{"title":"Neutrophil-mediated alteration of CXCL1/IL-8/AR signaling promotes prostate cancer cell proliferation","authors":"Zhifu Liu ,&nbsp;Yuxuan Tian ,&nbsp;Zheng Li ,&nbsp;Zhen Li ,&nbsp;Kehao Yang ,&nbsp;Yiming Zeng ,&nbsp;Jiao Hu ,&nbsp;Yuanwei Li ,&nbsp;Xiongbing Zu ,&nbsp;Shuai Hu","doi":"10.1016/j.yexcr.2025.114680","DOIUrl":"10.1016/j.yexcr.2025.114680","url":null,"abstract":"<div><div>The role of immune cells, particularly neutrophils, in the prostate cancer (PCa) progression remains poorly understood. In this study, we investigated the impact of neutrophils on PCa progression using an in vitro co-culture migration assay. Our findings revealed that PCa cells recruited more neutrophils than normal prostate epithelial cells. Importantly, the recruitment of neutrophils to PCa cells led to increased PCa cell proliferation. Further mechanistic investigations revealed that co-culture of PCa cells with neutrophils led to increased secretion of the chemokine CXCL1. This, in turn, stimulated neutrophils to produce the cytokine IL-8. The enhanced CXCL1/IL-8 signaling axis subsequently amplified androgen receptor (AR) signaling in PCa cells, thereby promoting their proliferation. Disruption of this pathway via IL-8 neutralizing antibodies or AR knockdown reversed the neutrophil-induced PCa cell proliferation. These findings were validated in a mouse model and further supported by clinical sample analysis. Collectively, our study highlights the therapeutic potential of targeting the newly identified signaling cascade involving infiltrating neutrophils within the PCa microenvironment. Understanding and modulating this pathway may offer novel strategies to suppress PCa progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114680"},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144670436","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}

{"title":"Comprehensive network pharmacology and experimental study to investigate the effects and mechanisms of Lophatherum gracile Brongn. for glioma treatment","authors":"Zelin Liu ,&nbsp;Lihua Dai ,&nbsp;Qian Jiang ,&nbsp;Simei Zhong ,&nbsp;Jiale Xiong ,&nbsp;Zhe Yang ,&nbsp;Ning Jing ,&nbsp;Yu-Hui Zhang ,&nbsp;Yan Ma","doi":"10.1016/j.yexcr.2025.114671","DOIUrl":"10.1016/j.yexcr.2025.114671","url":null,"abstract":"<div><h3>Background</h3><div>Gliomas are challenging to treat due to their invasive nature and resistance to conventional therapies. Recent study has revealed that <em>Lophatherum gracile Brongn.</em> extract has anti-cancer properties on fibrosarcoma cell. Nevertheless, its medicinal effects and mechanistic pathways on gliomas have not been explored.</div></div><div><h3>Aim of the study</h3><div>To investigate the detailed anti-glioma roles of <em>Lophatherum gracile Brongn.</em> extract and its specific pharmacological routes of action both <em>in vitro</em> and <em>in vivo</em>, focusing on autophagy, apoptosis, proliferation, and migration.</div></div><div><h3>Methods</h3><div>Ethanol extracts of <em>Lophatherum gracile Brongn.</em> were prepared, and the active compounds were appraised by high-performance liquid chromatography. Human glioma cells (A172, LN229, U-87 MG, and U251) were treated with various concentrations of the extract. Immunofluorescence and transmission electron microscopy were employed to investigate the autophagosomes. Cell viability, proliferation, migration, and death were assessed using various assays. The anti-tumor effects were further tested in animal models. Network pharmacology was employed to investigate the potential targets of the main compounds acting on glioma. Furthermore, RNA sequencing was conducted for transcriptome analysis and molecular docking was used for identification.</div></div><div><h3>Results</h3><div>The extract significantly attenuated glioma cell viability, proliferation, and migration, both <em>in vitro</em> and <em>in vivo</em>, while promoting autophagy, apoptosis, and cell death. Five active compounds were identified: chlorogenic acid, isoorientin, orientin, vitexin, and isovitexin. A total of 1472 glioma targets were identified, along with 219 drug targets for the five compounds. Combining analysis of differentially expressed genes revealed that dihydrofolate reductase may be a key target of these compounds, as determined by molecular docking analysis.</div></div><div><h3>Conclusions</h3><div><em>Lophatherum gracile Brongn.</em> extract exhibits significant anti-glioma effects in both cellular and animal models by targeting dihydrofolate reductase, providing novel insights into its therapeutic potential for glioma.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114671"},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616911","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}