Cell Biochemistry and Biophysics最新文献

{"title":"Dysregulation of the miR-1825/TSC2/mTOR Axis Contributes to Prostate Cancer Aggressiveness.","authors":"Ozel Capik","doi":"10.1007/s12013-026-02201-1","DOIUrl":"https://doi.org/10.1007/s12013-026-02201-1","url":null,"abstract":"<p><p>Prostate cancer (PCa) is the second most widespread cancer affecting solid tumor in men and the fifth most widespread cause of cancer-associated mortality in men. Research into the underlying molecular mechanisms of PCa is an urgent need to develop better therapeutic strategies and reveal new molecular targets for therapeutic intervention. In this study, we proposed to investigate the functional significance of miR-1825 in driving the malignant characteristics of PCa cells in relation to the TSC2/mTOR axis. We primitively examined the effects of miR-1825 mimic/inhibitor on cell viability, cell motility, and clonogenic ability of DU145, LNCaP, and PC3 PCa cells. Subsequently, we investigated the relationship between miR-1825 expression and the TSC2/mTOR signaling pathway through integrated in vitro and in silico approaches. Overexpression of miR-1825 increasingly suppressed TSC2 expression at both the mRNA and protein levels, while concomitantly increasing mTOR expression. In contrast, inhibition of miR-1825 led to the upregulation of TSC2 and a corresponding decrease in mTOR levels. These outcomes support that TSC2 is a putative target of miR-1825 and further confirm the inverse regulatory relationship between TSC2 and mTOR. Moreover, dysregulation of miR-1825 significantly enhanced cell viability, clonogenic ability, and cell motility in PCa cells. Collectively, these data indicate that miR-1825 promotes tumorigenic phenotypes through the dysregulation of the TSC2/mTOR signaling axis in PCa. In summary, our findings demonstrate that miR-1825 acts as an oncogenic regulator in PCa by targeting TSC2 and modulating the mTOR pathway. The miR-1825/TSC2/mTOR axis may represent a promising therapeutic target for the treatment of PCa.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antitumor Activity of Mitochondrial Uncouplers Based on Platinum (II) N-Heterocyclic Carbene Complexes.","authors":"Vsevolod V Melekhin, Maria D Tokhtueva, Anna E Chernysheva, Danil V Andreev, Svetlana M Podergina, Anastasia V Paramonova, Oleg G Makeev, Vladislav M Abramov, Oleg S Eltsov","doi":"10.1007/s12013-026-02181-2","DOIUrl":"https://doi.org/10.1007/s12013-026-02181-2","url":null,"abstract":"<p><p>In the present study, the effects of mitochondrial uncouplers on lung carcinoma cells were investigated. The compounds were found to inhibit cell proliferation by inducing cell cycle arrest at the G1/S transition. Treatment with the tested complexes led to acidification of the extracellular medium, associated with enhanced lactate production due to compensatory increase in glycolytic flux. The effect on HIF signalling has been demonstrated, which is especially intriguing when considering how to overcome neoplastic cells' resistance to chemical agents. Signaling pathway analysis revealed that mitochondrial uncoupling increased ERK1/2 phosphorylation levels, which may represent a compensatory cellular response to energy stress. Exposure to the complexes also resulted in elevated reactive oxygen species (ROS) generation and pronounced morphological alterations. These findings provide further insight into the mechanisms of action of mitochondrial uncouplers and their impact on proliferation, metabolism, and signaling pathways in tumor cells.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell-Type-Dependent Responses to Oleuropein in MDA-MB-231 Breast Cancer Cells and HUVECs.","authors":"Derya Okuyan, Ayla Solmaz Avcıkurt","doi":"10.1007/s12013-026-02178-x","DOIUrl":"https://doi.org/10.1007/s12013-026-02178-x","url":null,"abstract":"<p><p>Breast cancer progression is associated with dysregulation of cell survival, apoptosis, and cell-cycle control. Oleuropein (OL), a major secoiridoid constituent of olive-derived products, has attracted interest because of its diverse biological activities and potential relevance to cancer research. This study evaluated the cellular and molecular responses to OL in MDA-MB-231 triple-negative breast cancer cells and non-malignant human umbilical vein endothelial cells (HUVECs). Cell viability was assessed following exposure to 10-250 µg/mL OL for 24, 48, and 72 h. OL produced an exposure-time-dependent reduction in MDA-MB-231 cell viability, with estimated IC₅₀ values of >250 µg/mL at 24 h, 117.5 µg/mL at 48 h, and 26.42 µg/mL at 72 h. Based on the overall viability profiles of the two cell models, 100 µg/mL OL was selected for subsequent functional and molecular analyses. At this concentration, MDA-MB-231 viability progressively decreased with prolonged exposure, whereas HUVEC MTT-derived viability values were maintained. OL treatment reduced clonogenic capacity and wound closure in MDA-MB-231 cells, while increased clonogenic capacity and wound closure were observed in HUVECs. qRT-PCR analysis showed increased BAX and CDKN1B and reduced BCL2 expression in MDA-MB-231 cells, whereas HUVECs exhibited reduced BAX and increased BCL2 and CDKN1B expression. Western blot analysis revealed time-dependent changes in BAX, BCL-2, and p27 protein abundance, with partial directional correspondence to the transcriptional findings, particularly at later exposure times. Collectively, these findings indicate that OL elicits distinct cell type-dependent responses in malignant breast cancer and non-malignant endothelial cells. The coordinated viability, clonogenic, wound closure, and molecular expression profiles observed in MDA-MB-231 cells support further investigation of OL in breast cancer models, while the distinct HUVEC response highlights the need to clarify its endothelial and angiogenesis-related effects.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Umbilical Cord Mesenchymal Stem Cells Improve PINK1/PARKIN-Mediated Mitophagy Inhibition in Preeclampsia.","authors":"Nan Zhang, Shuqi Liu, Mengnan Li, Huijing Ma, Hong Yu, Jing Ji, Miao Xu, Lijun Yang, Ruidan Zhang, Hailan Yang","doi":"10.1007/s12013-026-02188-9","DOIUrl":"https://doi.org/10.1007/s12013-026-02188-9","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia (PE) is a progressive multisystem disorder that arises after 20 weeks of gestation and poses severe risks to both maternal and fetal health. Umbilical cord mesenchymal stem cells (UC-MSCs) exhibit antioxidant and pro-angiogenic properties, which have been shown to be effective in treating various diseases.</p><p><strong>Methods: </strong>HTR8/SVneo cells were induced by lipopolysaccharide (LPS) to establish a PE cell model. Western blot (WB) and real-time quantitative PCR (RT-qPCR) were conducted to detect the expression of genes related to mitophagy. Meanwhile, ATP level was detected using an ATP content assay kit and mitochondrial membrane potential (MMP) level was detected under a fluorescence microscope using an MMP detection kit. Next, a PE rat model was induced using N(ω)-nitro-l-arginine methyl ester (L-NAME), followed by UC-MSCs transplantation. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of PE biomarkers, and the expression of mitophagy related genes was assessed via RT-qPCR, WB, and immunohistochemistry.</p><p><strong>Results: </strong>UC-MSCs modulated the levels of Phosphatase and Tensin Homolog-induced Kinase 1 (PINK1), Parkin RBR E3 ubiquitin protein ligase (PARKIN), reversed the inhibition of mitophagy in the PE model and increased both ATP content and MMP. Importantly, UC-MSCs alleviated hypertension and proteinuria in PE rats, improved pregnancy outcomes, and mitigated the imbalance in angiogenesis.</p><p><strong>Conclusion: </strong>This study demonstrates that UC-MSCs improve PE trophoblast injury and vascularization imbalance through regulating mitochondrial autophagy. Our results indicate that UC-MSCs may hold significant potential for treating PE.Clinical trial number Not applicable.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ergothioneine Modulates Inflammatory Signaling in LPS-Stimulated RAW 264.7 Macrophages.","authors":"Neil Patrick Uy, Hyeonjun Yu, Chang-Dae Lee, Soon Yeong Park, Hoon Kim, Sanghyun Lee","doi":"10.1007/s12013-026-02179-w","DOIUrl":"https://doi.org/10.1007/s12013-026-02179-w","url":null,"abstract":"<p><p>Ergothioneine (EGT), a naturally occurring antioxidant abundant in Hericium erinaceus, has been implicated in inflammation-related disorders, including inflammatory bowel disease (IBD). A validated HPLC-DAD method was developed for EGT quantification in H. erinaceus, demonstrating satisfactory specificity, linearity, precision, and accuracy. Network pharmacology analysis identified shared targets between EGT-associated proteins and IBD-related genes, with HSP90AA1 emerging as a key candidate. Molecular docking revealed stable binding of EGT within the HSP90AA1 active site. In lipopolysaccharide-stimulated RAW 264.7 macrophages, EGT significantly reduced the expression of pro-inflammatory mediators, including inducible nitric oxide synthase and cyclooxygenase-2, while modulating PPARγ expression. These findings provide integrated chemical and mechanistic evidence supporting EGT as a bioactive constituent of H. erinaceus with potential relevance for modulating intestinal inflammation. However, further studies are required to validate its therapeutic relevance in disease-specific models.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EphA2 Silencing Attenuates IL-1β-Induced Chondrocyte Ferroptosis and Extracellular Matrix Degradation In Vitro.","authors":"Yan Chen, Wenbin Qian, Hui Zhu","doi":"10.1007/s12013-026-02183-0","DOIUrl":"https://doi.org/10.1007/s12013-026-02183-0","url":null,"abstract":"<p><p>This study investigated the role of erythropoietin-producing hepatocellular carcinoma receptor A2 (EphA2) in interleukin-1β (IL-1β)-induced chondrocyte injury and ferroptosis-associated alterations in osteoarthritis (OA). Primary rat chondrocytes were stimulated with IL-1β to establish an in vitro OA-like model. EphA2 was silenced using siRNA. Cell viability and apoptosis were assessed using MTT and TUNEL assays, respectively. Extracellular matrix (ECM) metabolism was evaluated by immunofluorescence and RT-qPCR. Ferroptosis-associated changes were assessed by measuring mitochondrial ferrous iron accumulation, intracellular Fe²⁺, malondialdehyde (MDA), glutathione (GSH), and the levels of ferroptosis-related proteins. IL-1β increased EphA2 expression, reduced collagen II and aggrecan expression, and increased the expression of disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5) and matrix metalloproteinase 13 (MMP-13). EphA2 silencing restored ECM homeostasis and attenuated the IL-1β-induced loss of viability and apoptosis. Moreover, EphA2 silencing reduced Fe²⁺ accumulation and lipid peroxidation, restored GSH levels, increased GPX4 and SLC7A11 expression, and decreased ACSL4 expression, consistent with the attenuation of ferroptosis-associated stress. EphA2 silencing attenuates IL-1β-induced chondrocyte injury, ECM dysregulation, and ferroptosis-associated alterations in vitro. EphA2 may contribute to ferroptosis-associated chondrocyte dysfunction in OA, warranting further mechanistic and in vivo studies.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Juanbi Qianggu Formula Alleviates Rheumatoid Arthritis by Suppressing the TNF-α/NF-κB Signaling Pathway.","authors":"Guowei Qiu, Junjie Wen, Zheng Xiang, Wei Hu, Xinyu A, Chenxin Gao, Yanqing Bian, Xirui Xu, Lu Meng, Lianbo Xiao","doi":"10.1007/s12013-026-02182-1","DOIUrl":"https://doi.org/10.1007/s12013-026-02182-1","url":null,"abstract":"<p><p>Juanbi Qianggu Formula (JBQGF) is a traditional Chinese medicine prescription with demonstrated clinical efficacy in rheumatoid arthritis (RA), yet its pharmacological mechanisms remain unclear. This study investigated whether JBQGF attenuates RA-associated inflammation by inhibiting the TNF-α/NF-κB signaling pathway. In a collagen-induced arthritis (CIA) mouse model, JBQGF significantly ameliorated joint swelling, bone erosion, and systemic inflammation, with efficacy comparable to methotrexate, and reduced serum and synovial TNF-α levels. In LPS-stimulated RAW 264.7 macrophages, JBQGF-containing serum suppressed NF-κB p65 nuclear translocation and downregulated TNF-α, iNOS, and COX-2 expression. Transcriptomic profiling of synovial tissue, coupled with functional rescue assays, revealed that JBQGF directly suppresses TNFAIP2 expression via the primary NF-κB axis rather than secondary TNF-α depletion, thereby disrupting an NF-κB/TNFAIP2/ROS inflammatory cascade. These findings indicate that JBQGF targets the TNF-α/NF-κB pathway at multiple nodes to restore cellular inflammatory and redox balance, providing a mechanistic basis for its therapeutic effects in RA.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk Between Nrf2 and Metabolic Pathways: Redox Regulation, Glutaminolysis, and Cellular Proliferation.","authors":"Rademene Sunday Oria, Amarachukwu Vivian Umeano, Victoria Onyemachi Chukwu, Happiness Ochi Inyang, Saviour God'swealth Usin","doi":"10.1007/s12013-026-02185-y","DOIUrl":"https://doi.org/10.1007/s12013-026-02185-y","url":null,"abstract":"<p><p>The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) was first described as a cytoprotective regulator that switches on antioxidant and detoxification genes through the antioxidant response element (ARE). That view is accurate but incomplete. Nrf2 also controls metabolic genes governing the pentose phosphate pathway, glutamine catabolism, regeneration of reduced nicotinamide adenine dinucleotide phosphate (NADPH), fatty acid handling, purine synthesis and iron storage, placing it where antioxidant defence and biosynthesis draw on shared pools of carbon, nitrogen and reducing equivalents. This critical narrative review, assembled purposively from PubMed, MEDLINE and Google Scholar rather than systematically, examines the Nrf2/Keap1 axis and then the point where Nrf2 partitions glutamate between anaplerotic entry into the tricarboxylic acid cycle and glutathione synthesis. Stable-isotope tracing shows this partitioning to be measurable as flux: Nrf2 activation raises both glutamate consumption for glutathione and glutamate export through system xc⁻, limiting the carbon available to central metabolism and creating dependency on exogenous glutamine. The same arithmetic accounts for tanshinone IIA starving proliferating myofibroblasts in pulmonary fibrosis and, in the diabetic heart, for Nrf2 repressing thioredoxin-interacting protein at an ARE to protect cardiomyocytes. We argue that the contested dual role of Nrf2 in tumour progression follows from this logic: Nrf2 supplies substrate rather than a proliferative instruction, so the direction of its effect is set by whether the cell carries demand able to consume that substrate and a checkpoint able to restrain its use. We close on tissue context and on matching Nrf2-directed compounds to tissue metabolic state.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Green Synthesis, Physicochemical Characterization, and In Vitro Biological Evaluation of Moringa concanensis-Mediated Zinc Oxide Nanoparticles with Keratinocyte Wound-Closure Activity.","authors":"Subhasini Kandasamy, Shanmugarathinam Alagarsamy","doi":"10.1007/s12013-026-02173-2","DOIUrl":"https://doi.org/10.1007/s12013-026-02173-2","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Oxidative stress, hyperglycaemia and defective keratinocyte-mediated repair impair diabetic wound healing. Moringa concanensis is a lesser explored medicinal plant with wide phytochemical constituents and feasible for the nanoparticle mediated biomedical applications. The current research was focused on the green synthesis of zinc oxide nanoparticles (ZnO NPs) with M. concanensis hydromethanolic leaf extract, their physicochemical characterization, and initial in vitro assessment of antioxidant, antidiabetic enzyme inhibitory, cytocompatibility, and wound-closure activities. ZnO NPs were synthesized using the hydromethanolic leaf extract of M. concanensis and zinc nitrate under alkaline conditions and characterized using UV-visible spectroscopy, Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), dynamic light scattering (DLS), zeta potential analysis, scanning electron microscopy with energy dispersive X-ray spectroscopy (SEM-EDX), high-resolution transmission electron microscopy (HRTEM), Raman spectroscopy and gas chromatography-mass spectrometry (GC-MS). The antioxidant activity was determined by DPPH, ABTS and FRAP assay, and the α-amylase and α-glucosidase inhibition assay were used as preliminary biochemical indicators for antidiabetic activity. Cytocompatibility was evaluated in HaCaT human keratinocytes, with the MTT assay. The wound-closure activity was evaluated by an in vitro scratch assay. The synthesized ZnO NPs showed a characteristic UV-visible absorption maximum at 364 nm with an estimated optical band gap of 3.40 eV. The XRD confirmed the crystalline hexagonal wurtzite ZnO phase with an average crystallite size of about 35 nm and the Raman spectrum showed the characteristic E₂(high) mode at 438 cm-1. DLS showed an average hydrodynamic diameter of 245.2 nm, a polydispersity index of 0.540 and a zeta potential of -12.0 mV. From EDX analysis, the wt% of Zn and O was 69.54 and 30.46 respectively. HRTEM and SAED indicated that the nanoparticles were mostly hexagonal/polyhedral with clear lattice fringes. GC - MS analysis of M. concanensis extract showed tentative identification of 78 phytochemical constituents. The antioxidant activity of ZnO NPs was found to be concentration dependent with IC50 values of &gt; 100 µg/mL, 74.6 µg/mL and 64.20 µg/mL for DPPH, ABTS and FRAP respectively. The IC 50 values for α-amylase and α-glucosidase inhibition were 86.53 and 72.95 µg/mL, respectively. The viability of HaCaT cells was &gt; 50% in the concentration range tested (100-1000 µg/mL), which corresponds to an estimated IC₅₀ &gt; 1000 µg/mL. ZnO NPs at 584 µg/mL (85.00 ± 1.05%) showed significantly increased scratch wound closure compared to control (61.71 ± 0.89%) after 48 h (p = 0.0017). All quantitative experiments were performed with appropriate replicates and are expressed as mean ± standard deviation. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparison test or an unpaired Student's t","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes Derived from Non-small Cell Lung Cancer Cells Transfer LINC00467 to Induce the Proliferation of Cancer-associated Fibroblasts.","authors":"Zengyao Li, Yan Wu, Sen Niu, Yanhua Chang, Rongguo Lu, Tao Bian, Jing Liu","doi":"10.1007/s12013-026-02170-5","DOIUrl":"https://doi.org/10.1007/s12013-026-02170-5","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) significantly contribute to non-small cell lung cancer (NSCLC) progression by remodeling the extracellular matrix and mediating paracrine signaling. Although exosomal lncRNAs are key regulators of tumor-stroma interactions, the specific functions of individual lncRNAs remain poorly understood. LINC00467 and miR-133b were selected for further investigation in this study based on previous reports, prior evidence of lncRNA-miRNA interaction, and preliminary experimental observations in NSCLC-derived exosomes and fibroblast activation models. Exosomes from A549 and primary NSCLC cells were isolated using a polymer-based precipitation method and validated by Western blotting. LINC00467 was silenced via siRNA, and isolated exosomes were co-cultured with MRC5 fibroblasts and CAFs. Fibroblast activation and proliferation markers were assessed by Western blotting and cell counting kit assays. miR-133b involvement was examined using quantitative real-time PCR and inhibitor-based rescue experiments. Exosome-pretreated MRC5 fibroblasts were also co-cultured with A549 cells. Exosomal LINC00467 was enriched in NSCLC-derived exosomes. Knockdown of LINC00467 in NSCLC cells reduced its exosomal levels, leading to decreased expression of activation markers (α-SMA, COL-I, COL-III) and cell cycle regulators (Cyclin B1, Cyclin D1) in recipient fibroblasts. In addition, exosomes with LINC00467 knockdown inhibited the cell proliferation of fibroblasts. It was also revealed that LINC00467-deficient exosomes upregulated miR-133b expression. Importantly, inhibition of miR-133b reversed the suppressive effects of LINC00467 knockdown. Exosome-pretreated fibroblasts enhanced A549 cell proliferation, colony formation, and migration in vitro. This study identifies a novel exosomal LINC00467/miR-133b axis that promotes fibroblast activation and proliferation in NSCLC.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}