Cytotechnology最新文献

{"title":"Anticancer potential of Viola cornuta-derived green-synthesized CuO nanoparticles via ROS-induced apoptosis in breast cancer cell lines.","authors":"Maryam Fekri Soufiabadi, Mahsa Ziasistani, Hannaneh Bazgir, Shahrzad Eftekhar Vaghefi, Narges Karimi, Shahriar Dabiri","doi":"10.1007/s10616-026-01013-8","DOIUrl":"https://doi.org/10.1007/s10616-026-01013-8","url":null,"abstract":"<p><p>Breast cancer is associated with significant mortality amongst women universally. Common treatments face various difficulties, including the development of drug resistance. This fact necessitates the exploration of new therapeutic protocols. Our study evaluated the apoptotic effects of green-synthesized copper oxide nanoparticles (CuO-NPs) on breast cancer cells (MCF7) compared to normal epithelial cells (MCF10) through a series of in vitro assays. Copper oxide nanoparticles were obtained from Viola corneta leaves. The crystalline structure and spherical morphology of the nanoparticles were represented by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy (SEM). Cells were treated with multiple concentrations of CuO-NPs. Cell viability assay revealed dose-dependent IC50 values of 35.4 µg/mL and 85 µg/mL for MCF7 and MCF10A, respectively. CuO-NPs remarkably promoted ROS production and induced apoptosis, as evidenced by Annexin V/PI staining. Flow cytometric analysis exhibited a marked rise in the SubG1 phase of the cell cycle in the MCF7 population. Ultimately, real-time PCR analysis also exhibited a higher expression of pro-apoptotic than anti-apoptotic genes in treated cells. These findings emphasize the ability of CuO-NPs to induce apoptosis in breast cancer cell lines and highlight their effectiveness in selectively targeting the cancer cells rather than the normal cells.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"164"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The miR-99b-3p/<i>BMP8A</i> axis in poor healing of osteoporotic femoral neck fractures.","authors":"Ke Ma, Congcong Shi, Tongbao Dong, Shengqian Wang, Zhibiao Wang","doi":"10.1007/s10616-026-01048-x","DOIUrl":"https://doi.org/10.1007/s10616-026-01048-x","url":null,"abstract":"<p><p>Impaired healing of osteoporotic femoral neck fractures is a serious problem facing the clinic. There is a lack of effective preoperative prognostic indicators, and the underlying molecular mechanisms require further exploration. In this retrospective cohort study, 160 patients with osteoporotic femoral neck fractures were enrolled, with 71 exhibiting poor healing and 89 normal healing. Serum samples were collected upon admission, prior to surgery. Expression of miR-99b-3p and <i>BMP8A</i> was detected via qRT-PCR. The preliminary discriminatory ability of miR-99b-3p was evaluated using ROC curves. The effects of miR-99b-3p on cell viability and osteogenic activity in MC3T3-E1 and hBMSCs were assessed using CCK-8, while osteogenic marker expression (RUNX2, ALP, FN1, Osteocalcin) was analyzed via qPCR, and protein-level mechanistic validation was performed via Western blotting. Targeting of the <i>BMP8A</i> 3'UTR by miR-99b-3p was validated via dual-luciferase assay. Serum miR-99b-3p was significantly upregulated in patients with poor healing (<i>P</i> < 0.001) and showed a significant negative correlation with <i>BMP8A</i> (Adjusted partial <i>r</i> = -0.755, <i>P</i> < 0.001). ROC analysis indicated that serum miR-99b-3p showed preliminary discriminatory ability for identifying poor healing (AUC = 0.859, 95% CI: 0.800-0.917, optimal cutoff = 1.22). Inhibition of miR-99b-3p promoted <i>BMP8A</i> expression, enhanced cell viability, and upregulated osteogenic markers (all <i>P</i> < 0.01), while BMP8A knockdown reversed these effects at both the functional and protein levels. Serum miR-99b-3p represents an exploratory prognostic indicator for poor healing in osteoporotic femoral neck fractures, likely impairing osteogenesis via the <i>BMP8A</i> regulatory axis.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"178"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated network pharmacology and in vitro/in silico evaluation of the bioactive potential of <i>Gundelia komagenensis</i> fırat extracts.","authors":"Abdülmelik Aras, Yunus Dağhan, Alpaslan Bayrakdar, İlhan Sabancilar, Ercan Oğuz, Fikret Türkan, Mustafa Yaşar, Ömer Kiliç, Şinasi Yıldırımlı","doi":"10.1007/s10616-026-01053-0","DOIUrl":"https://doi.org/10.1007/s10616-026-01053-0","url":null,"abstract":"<p><p><i>Gundelia komagenensis</i> Fırat, an endemic member of the Asteraceae family, was investigated for its phytochemical composition, antioxidant, enzyme inhibitory, cytotoxic, and computationally predicted pharmacological properties. Methanol (MeOH) and dichloromethane (DCM) extracts prepared from the aerial parts of <i>Gundelia komagenensis</i> were evaluated using ABTS and FRAP antioxidant assays, enzyme inhibition tests against acetylcholinesterase (AChE), α-glucosidase, and α-amylase, LC-MS/MS profiling, MTT-based cytotoxicity assays, and integrated in silico analyses. Both extracts exhibited antioxidant activity; among the extracts, DCM had a lower ABTS IC₅₀ value than MeOH (13.7 vs.14.5 µg/mL). DCM also had lower IC₅₀ values for AChE, α-glucosidase, and α-amylase than MeOH (1.132-1.372 µg/mL). LC-MS/MS revealed solvent-dependent profiles, with chlorogenic acid, vanillin, trans-cinnamic acid, and gentisic acid predominating in MeOH, and vanillin, trans-cinnamic acid, and luteolin in DCM. The MeOH extract of <i>G. komagenensis</i> did not exhibit significant cytotoxicity against either MIA PaCa-2 or HUVEC cells. In contrast, the DCM extract reduced MIA PaCa-2 cell viability in a concentration-dependent manner while exerting relatively limited effects on HUVEC cells, suggesting a selective cytotoxicity tendency under the tested conditions. Computational analyses identified chlorogenic acid as the most promising bioactive constituent. Molecular docking showed the highest binding affinities toward AChE, α-glucosidase, and α-amylase, while molecular dynamics simulations and MM-GBSA calculations supported the stability of the corresponding protein-ligand complexes. Network pharmacology suggested that the identified phenolics may regulate disease-related pathways through AP-1/NF-κB-associated targets. Chlorogenic acid emerged as a key multi-target candidate warranting further experimental validation.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"180"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13476198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of miR-23b-3p improves the intestinal mucosal barrier function in LPS-induced intestinal epithelial inflammatory injury models via modulating Erbin.","authors":"Guangquan Zhou, Xiao Sun, Feng Jin, Junbo Yang, Na Ding","doi":"10.1007/s10616-026-01050-3","DOIUrl":"10.1007/s10616-026-01050-3","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a persistent inflammation of the gastrointestinal tract that severely affects patients' quality of life. miRNAs are associated with the pathogenesis of IBD. Nevertheless, the mechanism of miR-23b-3p and IBD has yet to be elucidated. The aim of this study was to investigate the potential clinical diagnostic value of miR-23b-3p and its related molecular mechanisms. LPS was utilized to construct an LPS-induced intestinal epithelial inflammatory injury model in vitro. RT-qPCR was employed to measure the levels of miR-23b-3p and Erbin. The MTT assay was applied to detect cell viability. ELISA was performed to monitor the inflammation factor levels. The fluorescein isothiocyanate-dextran assay was employed to assess permeability. Dual-luciferase reporter assay was performed to validate the targeting relationship. The level of miR-23b-3p was elevated in patients with ulcerative colitis (UC) and Crohn's disease (CD) and it showed promising diagnostic ability for IBD. Furthermore, miR-23b-3p showed positive correlations with the Mayo score in UC patients and the CDAI score in CD patients. In terms of mechanism, miR-23b-3p inhibitor enhanced cell viability and TEER as well as reduced proinflammatory factor levels and FITC-dextran permeability in the LPS-induced intestinal epithelial inflammatory injury model, which was reversed by si-Erbin. These findings suggest that miR-23b-3p may contribute to intestinal epithelial inflammatory injury and barrier dysfunction, at least partly through regulation of Erbin.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01050-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"183"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13493739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Borneol-based nanoparticles encapsulating Doxorubicin/Sodium tanshinone IIA sulfonate enhance the effect of anti-glioma and alleviate cardiotoxicity.","authors":"Xiaoli Ye, Jingying Li, Qing Song, Jia He, Yuye Huang","doi":"10.1007/s10616-026-01054-z","DOIUrl":"10.1007/s10616-026-01054-z","url":null,"abstract":"<p><p>Clinical treatment of brain glioma remains challenging due to chemotherapeutic resistance, cardiotoxicity and the presence of blood-brain barrier (BBB). Advanced nanoplatforms that can cross the BBB efficiently and target brain glioma with lower cardiotoxicity are urgently needed. Herein, the protective effect of borneol-based nanoparticles encapsulating Doxorubicin/Sodium tanshinone IIA sulfonate (BO-Dox/STS-NPs) on glioma was explored. BO-Dox/STS-NPs were comprehensively evaluated by measuring their particle size, encapsulation efficiency, and drug-loading capacity. Pharmacokinetic studies evaluated their concentrations in animal serum and brain. In an orthotopic rat glioma model, the antitumor efficacy and cardioprotective effects of Dox, Dox/STS, Dox/STS-NPs, BO-Dox/STS-NPs, and Dox-NPs were compared. In vitro, U87 cells were treated with these formulations, and antitumor effects were assessed via CCK8 assay, flow cytometry, migration assay, and colony formation assay. In orthotopic glioma rat models, treatment with BO-Dox/STS-NPs resulted in superior tumor inhibition and increased tumor cell apoptosis compared to other formulations. Furthermore, BO-Dox/STS-NPs significantly alleviated doxorubicin-induced cardiotoxicity, as evidenced by improved myocardial pathology, reduced left ventricular end-diastolic pressure, and decreased levels of cardiac injury markers (cTnI, CK) and oxidative stress indicators (LDH, MDA), alongside enhanced antioxidant capacity (SOD) and mitochondrial membrane potential. In vitro, BO-Dox/STS-NPs exhibited the greatest uptake of Dox, the strongest inhibitory effects on U87 cell proliferation, migration, and colony formation, and promoted apoptosis more effectively than other treatment groups. Co-loading Dox and STS into borneol-modified nanoparticles enables effective treatment of glioma while reducing cardiotoxicity. This approach contributes to the development of a versatile technological platform for constructing diverse brain-targeted nanocarriers.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"185"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SOX4 facilitates osteogenic differentiation through suppressing NLRP3 transcription-mediated pyroptosis.","authors":"Ping Li, Xue-Yi Lin, Yu Lin, Yan Liu, Wei-Bing Yang","doi":"10.1007/s10616-026-01040-5","DOIUrl":"10.1007/s10616-026-01040-5","url":null,"abstract":"<p><p>SOX4 participates in cell differentiation, but its regulatory function and underlying mechanism in the osteogenic differentiation of MC3T3-E1 cells remain elusive. Immunofluorescence staining was used to detect SOX4 subcellular localization and co-localization with NLRP3. Alizarin Red staining was applied to evaluate osteogenic differentiation. RT-PCR and Western blot assays quantified mRNA and protein levels of SOX4, osteogenic markers (OPN, OCN, RUNX2), inflammatory cytokines, and pyroptosis-related proteins (NLRP3, caspase-1, GSDMD). JASPAR predicted SOX4 binding sites in the NLRP3 promoter and ChIP-qPCR was used to validate it. Dual-luciferase reporter assay was applied to assesse transcriptional regulation. Rescue experiments were performed via co-transfection of SOX4 and NLRP3 overexpression vectors. SOX4 was upregulated during MC3T3-E1 osteogenic differentiation. SOX4 overexpression reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), increased IL-10, and inhibited pyroptosis. SOX4 directly bound to the NLRP3 promoter to suppress its transcription. NLRP3 overexpression reversed SOX4-induced enhancement of osteogenic differentiation and marker expression. SOX4 promotes MC3T3-E1 osteogenic differentiation by directly inhibiting NLRP3 transcription, thereby regulating inflammation and pyroptosis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01040-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"172"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PCDHGB2 promotes docetaxel resistance in prostate cancer via TR4-mediated activation of the HIF-1α/VEGFA pathway.","authors":"Fanyu Meng, Xinyi Zhou, Yong Qin, Pengju Liu","doi":"10.1007/s10616-026-01051-2","DOIUrl":"https://doi.org/10.1007/s10616-026-01051-2","url":null,"abstract":"<p><p>Prostate cancer poses a significant threat to men's health worldwide. Docetaxel (DTX) remains a cornerstone chemotherapeutic agent for PC, yet the emergence of docetaxel resistance has critically compromised clinical outcomes. Elucidating the molecular mechanisms underlying docetaxel resistance and identifying novel therapeutic targets are therefore imperative. This study integrated transcriptomic profiles and clinical data from the The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD) and Gene Expression Omnibus (GEO) databases to identify <i>PCDHGB2</i> as a pivotal gene associated with docetaxel resistance. Bioinformatics analyses were systematically conducted to evaluate correlations between <i>PCDHGB2</i> expression, tumor microenvironment heterogeneity, clinicopathological characteristics, and patient prognosis. Experimental validation included quantitative real-time PCR (RT-qPCR) and immunofluorescence for expression profiling, Cell Counting Kit-8 (CCK-8) assays for cellular viability assessment, alongside co-immunoprecipitation and molecular docking to characterize protein interactions. Our findings demonstrate that PCDHGB2 serves as a central mediator of docetaxel resistance in PC, exhibiting significant associations with tumor microenvironment heterogeneity. Spatial analysis revealed differential <i>PCDHGB2</i> distribution across prostate carcinoma cell subtypes, correlating with tumor invasiveness. Mechanistically, PCDHGB2 directly binds to testicular receptor 4 (TR4), stabilizing its expression and subsequently activating the hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor A (VEGFA) signaling axis to drive chemoresistance. To our knowledge, this study provides an initial comprehensive analysis of PCDHGB2's functional role in prostate cancer, uncovers a poorly recognized epigenetic mechanism of docetaxel resistance, and suggests a theoretical framework for improving prognostic strategies in prostate cancer patients.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01051-2.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"181"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of tetrandrine on the i<i>n vitro</i> proliferation and differentiation of black sea bream (<i>Acanthopagrus schlegelii</i>) myogenic cell lines.","authors":"Chae Wan Kang, Eun Soo Jeong, Dan Hee Han, Jae Hoon Choi, Seung Pyo Gong","doi":"10.1007/s10616-026-01061-0","DOIUrl":"https://doi.org/10.1007/s10616-026-01061-0","url":null,"abstract":"<p><p>Teleost myogenesis differs from mammalian systems, and well-characterized fish myogenic cell models remain limited. Tetrandrine, a bisbenzylisoquinoline alkaloid, impairs myogenesis and induces atrophy-associated responses in mammalian models, but its effects on teleost myogenic cells remain unclear. This study examined tetrandrine responses in black sea bream (<i>Acanthopagrus schlegelii</i>) myogenic cell lines. Cells were treated with tetrandrine to assess cytotoxicity, proliferative growth, myogenic differentiation, and associated cellular responses. Tetrandrine showed concentration-dependent cytotoxicity at higher concentrations, and 1, 3, and 5 µM were selected for subsequent experiments. Under growth conditions, tetrandrine exerted modest, cell line-dependent effects on proliferation. In contrast, tetrandrine markedly inhibited myogenic differentiation, as shown by reduced myotube formation, decreased fusion index, and suppressed expression of myogenic regulatory genes, including <i>Pax7</i>, <i>MyoD</i>, <i>Myog</i>, and <i>MyHC</i>. To examine whether proteolytic or oxidative stress-related processes contributed to this phenotype, cells were co-treated with MG-132, chloroquine, or N-acetylcysteine. These treatments did not restore tetrandrine-impaired myotube fusion, although MG-132 partially restored <i>MyHC</i> expression and tetrandrine induced a cell line-dependent increase in intracellular ROS. Fluo-4-based Ca²⁺ measurements further showed that acute tetrandrine treatment attenuated KCl-induced Ca²⁺ responses in differentiated cells, whereas undifferentiated cells showed little change. These findings suggest that altered depolarization-linked Ca²⁺ handling may contribute to tetrandrine-associated inhibition of myogenic differentiation in this teleost cell system.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01061-0.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"193"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14 knockdown alleviates inflammation in oral lichen planus by driving macrophage M2 polarization through mediating FDX1 m6A modification.","authors":"Xuan-Jiang Shen, Jun Luo, Yu-Kang Ying, Hai-Qian Zhu","doi":"10.1007/s10616-026-00981-1","DOIUrl":"https://doi.org/10.1007/s10616-026-00981-1","url":null,"abstract":"<p><p><i>Background</i> Oral lichen planus (OLP) is a prevalent chronic disease affecting the oral mucosa, and its pathogenesis remains not fully understood. This study aims to examine the regulatory mechanism of METTL14/FDX1 in the development of OLP. <i>Methods</i> Macrophage polarization and METTL14/FDX1 expression were analyzed in mucosal tissues from OLP patients and controls via immunofluorescence, RT-qPCR, and ELISA. In vitro, THP-1-derived macrophages were transfected with METTL14 or FDX1 targeting/overexpression vectors to assess their roles in polarization (flow cytometry) and cytokine secretion (ELISA). The METTL14-FDX1 interaction and m6A modification were confirmed by RIP and MeRIP-PCR. Functional outcomes were evaluated in a macrophage-keratinocyte co-culture system (flow cytometry) and in an imiquimod-induced OLP mouse model treated with sh-METTL14. <i>Results</i> The abnormal accumulation of M1 macrophage was identified in mucosa of OLP patients. Upregulation of m6A-related key enzyme METTL14 was identified in macrophages of OLP patients, which was associated with inflammation of OLP. Mechanically, METTL14 knockdown reduced mRNA stability of FDX1 through m6A modification, thereby limiting the transcriptional expression of FDX1 in macrophage. Functionally, METTL14 overexpression promoted macrophage M1 polarization through upregulating FDX1. Additionally, macrophages with METTL14 knockdown inhibited keratinocytes apoptosis by polarizing to M2. In vivo, METTL14 knockdown alleviated inflammation in OLP mouse model by driving macrophage M2 polarization. METTL14, via upregulating FDX1, also promoted the production of T-helper cell-associated inflammatory cytokines (IFN-γ, IL-17) integral to OLP pathology. <i>Conclusion</i> METTL14 knockdown alleviates inflammation in OLP by driving macrophage M2 polarization through mediating FDX1 m6A modification.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"177"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13469019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming in pancreatic cancer: interplay of glucose, lipid, and amino acid metabolism in tumor progression.","authors":"Zeliang Zhang, Ying Tian, Bo Zhang, Kexiang Zhu","doi":"10.1007/s10616-026-01052-1","DOIUrl":"https://doi.org/10.1007/s10616-026-01052-1","url":null,"abstract":"<p><p>Pancreatic cancer is one of the most malignant solid tumors, with a five-year survival rate of less than 10%. The therapeutic challenges primarily stem from difficulties in early diagnosis, high heterogeneity, and extensive resistance to chemotherapy, targeted therapy, and immunotherapy. Recent studies have revealed that metabolic reprogramming, a core hallmark of cancer, is a key mechanism driving the malignant phenotype of pancreatic cancer, persisting throughout its initiation, progression, and development of treatment resistance. This article systematically reviews the molecular mechanisms underlying the dysregulation of three major nutrient metabolic pathways-glucose, lipid, and amino acid metabolism-and their interconnected regulatory networks. Regarding glucose metabolism, enhanced aerobic glycolysis and PPP activation collectively support tumor growth, redox maintenance, and microenvironmental remodeling, whereas lactate accumulation further contributes to immune evasion. Lipid metabolic reprogramming is characterized by coordinated alterations in de novo synthesis, fatty acid oxidation, and cholesterol homeostasis, which collectively regulate membrane remodeling, stemness maintenance, and therapeutic resistance. Amino acid metabolism is characterized by glutamine dependency and branched-chain amino acid metabolic reprogramming, which collectively support biosynthesis, redox homeostasis, and tumor adaptation. These three major metabolic pathways do not operate in isolation but form a dynamic, interconnected network. This network confers robust metabolic plasticity and adaptability to the tumor, constituting a fundamental basis for treatment resistance. Concurrently, stromal cells and immune cells within the tumor microenvironment also undergo metabolic reprogramming, forming a metabolic symbiotic system with cancer cells that further exacerbates treatment resistance. Although combination strategies targeting metabolic pathways-such as glycolysis inhibitors combined with gemcitabine, statins synergizing with chemotherapy, or metabolic interventions combined with immunotherapy-have shown promise in preclinical models, clinical translation remains challenging. These challenges arise from multiple factors, including tumor heterogeneity, metabolic compensation, drug delivery limitations, and the complexity of the tumor microenvironment. Future efforts should integrate single-cell metabolomics, organoid models, and multimodal imaging technologies to advance precision therapy based on metabolic subtyping. Additionally, the development of novel nanodelivery systems and multi-target combination regimens is needed to bridge the gap from mechanistic understanding to clinical application. Metabolic intervention holds potential not only for advanced-stage treatment but also for chemoprevention at the precancerous lesion stage, offering a novel approach to improving the prognosis of pancreatic cancer.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"179"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13476433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}