Cytotechnology最新文献

Correction: Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes. 校正：TNF-α通过NF-κB对大鼠皮质星形胶质细胞的神经营养调节作用。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-04-03 DOI: 10.1007/s10616-025-00743-5

Jaldeep Langhnoja, Lipi Buch, Prakash Pillai

引用次数: 0

Functional changes in β-lactoglobulin by conjugation with carboxymethyl cellulose. β-乳球蛋白与羧甲基纤维素偶联的功能改变。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-03-15 DOI: 10.1007/s10616-025-00741-7

Tatsuya Arai, Moeko Ono, Maiko Yoneda, Marika Sugamura, Tadashi Yoshida, Makoto Hattori

{"title":"Functional changes in β-lactoglobulin by conjugation with carboxymethyl cellulose.","authors":"Tatsuya Arai, Moeko Ono, Maiko Yoneda, Marika Sugamura, Tadashi Yoshida, Makoto Hattori","doi":"10.1007/s10616-025-00741-7","DOIUrl":"10.1007/s10616-025-00741-7","url":null,"abstract":"β-lactoglobulin (BLG) and carboxymethylcellulose (CMC) were conjugated by using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC). The BLG-CMC conjugates with different CMC content and molecular weights were prepared. Confirmation of conjugation was carried out by SDS-PAGE. CD spectra revealed that the secondary structure of BLG had maintained in the conjugates. Fluorescence studies indicated that the conformation around Trp had not changed in the conjugates. Retinol-binding activity indicated that the retinol-binding site of BLG changed by the conjugation. Equilibrium constants (KAS) of anti-BLG monoclonal antibodies (mAbs) to BLG after conjugating with CMC by competitive ELISA indicated that the structure around 15Val-29Ile and 8Lys-19Trp maintained their native structure, and the structure around 125Thr-135Lys changed by conjugation. By conjugation with CMC, emulsifying property of BLG in the acidic pH region and in the presence of NaCl were much improved. Because acidic pH and salt are frequently used in food, the BLG-CMC conjugates are considered to be useful for food applications. Immunogenicity of BLG in BALB/c mice was reduced by this conjugation. In particular, there was a marked improvement in both emulsifying property and reduced immunogenicity in the BLG-high molecular weight (HMW) CMC conjugate. Therefore, conjugation with CMC is an effective way to improve BLG's function, and CMC with a high molecular weight is preferable.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"79"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647329","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}

引用次数: 0

PRELP regulated by GAS5/miR-3127-5p suppresses cisplatin resistance in oral squamous cell carcinoma. GAS5/miR-3127-5p调控的PRELP抑制口腔鳞状细胞癌顺铂耐药

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-04-28 DOI: 10.1007/s10616-025-00749-z

Xiaoni Sun, Yang Liu, Luyi Chai, Jianbo Zhou

{"title":"PRELP regulated by GAS5/miR-3127-5p suppresses cisplatin resistance in oral squamous cell carcinoma.","authors":"Xiaoni Sun, Yang Liu, Luyi Chai, Jianbo Zhou","doi":"10.1007/s10616-025-00749-z","DOIUrl":"https://doi.org/10.1007/s10616-025-00749-z","url":null,"abstract":"Our previous study has identified that PRELP inhibits the progression of oral squamous cell carcinoma (OSCC). This study aimed to investigate the influence of PRELP on cisplatin (DDP) resistance in OSCC cells and to elucidate the underlying mechanism. The levels of PRELP, miR-3127-5p, and GAS5 in established DDP-resistant OSCC cell lines (CAL27/DDP and SCC-15/DDP) and parental cells were detected. Following transfection with PRELP overexpressing or silencing plasmids in DDP-resistant OSCC cells, DDP resistance was evaluated by the IC50 values, proliferation, apoptosis and ABCB1 expression. Bioinformatic analysis, dual-luciferase reporter assays, and rescue experiments were employed to explore the upstream miRNA and lncRNA of PRELP. Our results demonstrated that in both DDP-resistant cells, PRELP and GAS5 levels were decreased, while miR-3127-5p expression was increased compared with parental cells. PRELP overexpression reduced the IC50 of DDP and EdU-positive cell number, enhanced cell apoptosis, and suppressed ABCB1 expression in resistant cells. Conversely, PRELP silencing caused opposite effects. In the TCGA database, miR-3127-5p was highly expressed in HNSC, and patients with higher miR-3127-5p expression had shorter overall survival. A negative correlation was observed between miR-3127-5p and PRELP in HNSC. miR-3127-5p promoted DDP resistance in OSCC by targeting PRELP. GAS5 positively modulated PRELP expression by sponging miR-3127-5p. The alleviation of DDP resistance by GAS5 was attenuated by miR-3127-5p mimic and PRELP downregulation. In conclusion, PRELP, which is regulated by lncRNA GAS5/miR-3127-5p axis, suppresses DDP resistance in OSCC through decreasing ABCB1 expression. Targeting the GAS5/miR-3127-5p/PRELP axis may offer a promising strategy to overcome DDP resistance in OSCC.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00749-z.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"92"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972764","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}

引用次数: 0

PLGA microspheres loaded with si-circETS1 as a therapeutic strategy to delay intervertebral disc degeneration. 装载si-circETS1的PLGA微球作为延迟椎间盘退变的治疗策略。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-05-14 DOI: 10.1007/s10616-025-00768-w

Wenlei Nie, Rong Zhang, Pingfeng Xie, Min Yang, Jiaming Wu

{"title":"PLGA microspheres loaded with si-circETS1 as a therapeutic strategy to delay intervertebral disc degeneration.","authors":"Wenlei Nie, Rong Zhang, Pingfeng Xie, Min Yang, Jiaming Wu","doi":"10.1007/s10616-025-00768-w","DOIUrl":"https://doi.org/10.1007/s10616-025-00768-w","url":null,"abstract":"Intervertebral disc degeneration (IDD) is one of the leading causes of chronic low back pain and functional impairment, severely affecting the quality of life of patients. In recent years, circular RNA (circRNA), has gained attention for its critical role in cellular function regulation, especially its potential therapeutic effects in IDD. This study aims to elucidate the function of circETS1 in nucleus pulposus cells (NPCs) and develop a novel targeted therapeutic strategy. CircETS1, which was abnormally highly expressed in degenerated nucleus pulposus tissue, was identified through circRNA sequencing (circRNA-seq). The circular nature of circETS1 was confirmed by Sanger sequencing, RNase R digestion, and fluorescence in situ hybridization (FISH). Primary human NPCs were cultured, and the effects of regulating circETS1 on cell proliferation, apoptosis, and extracellular matrix metabolism were studied using reverse transcription quantitative polymerase chain reaction (RT-qPCR), Western blotting, flow cytometry, and immunofluorescence. Polylactic-co-glycolic acid (PLGA) microspheres (MS) loaded with si-circETS1 were prepared, and their therapeutic effects were evaluated. PLGA MS loaded with si-circETS1 effectively delivered si-circETS1 to nucleus pulposus tissue in both in vitro and in vivo experiments, significantly downregulating circETS1 expression, reducing inflammation, promoting extracellular matrix synthesis and repair, and ultimately delaying the progression of IDD. Consequently, PLGA MS loaded with si-circETS1 present an innovative and promising therapeutic strategy for IDD, demonstrating strong potential for clinical application.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"99"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12075713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076446","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}

引用次数: 0

cPLA₂α on the influence of Th17 and its role in the formation of liver fibrosis. cPLA2α对Th17的影响及其在肝纤维化形成中的作用。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-04-08 DOI: 10.1007/s10616-025-00750-6

Lina Ma, Wei Wang, Limin Gu, Liyun Wang

{"title":"cPLA2α on the influence of Th17 and its role in the formation of liver fibrosis.","authors":"Lina Ma, Wei Wang, Limin Gu, Liyun Wang","doi":"10.1007/s10616-025-00750-6","DOIUrl":"https://doi.org/10.1007/s10616-025-00750-6","url":null,"abstract":"This study primarily investigated the mechanism and pathways of the cPLA2α signaling pathway on Th17-mediated HSC activation and liver fibrosis, providing insights for clinical strategies to target HSC activation and delay the rapid progression of liver fibrosis. In vitro and in vivo model were established, and different concentrations of the cPLA2α inhibitor AACOCF3 were administered respectively for intervention. The expression of IL- 17 was detected by ELISA, and the expression of cPLA2α protein and HSC activation protein α-SMA index were detected by Western blot and immunofluorescence. In addition, observe the changes in the degree of liver fibrosis in mice through the pathological staining of mouse livers. In an in vitro system, Th17 could induce HSC activation. And after intervention, the results showed that the inhibitor could inhibit Th17 activation of HSC. Next, in an in vivo model, Th17 could also induce HSC activation. And after intervention, the results showed that the inhibitor could also inhibit HSC activation by Th17. Observation under liver pathological staining showed that the inflammation and staining were significantly reduced in the intervention group, suggesting a therapeutic effect of AACOCF3. Using in vitro and in vivo approaches, these data suggest that Th17 cells can promote the activation and proliferation of HSCs, which further exerts a role in promoting liver fibrosis. These data also suggest that the cPLA2α pathway may be involved in the activation of HSCs by Th17 cells and induce liver fibrosis mechanisms.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"87"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969431","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}

引用次数: 0

Exosomes derived from human umbilical cord blood mesenchymal stem cells protect against blue light-induced damage to retinal pigment epithelial cells by inhibiting FGF2 expression. 来自人脐带血间充质干细胞的外泌体通过抑制FGF2的表达来保护视网膜色素上皮细胞免受蓝光诱导的损伤。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-04-09 DOI: 10.1007/s10616-025-00752-4

Guang-Ming Liu, Yan Liu

{"title":"Exosomes derived from human umbilical cord blood mesenchymal stem cells protect against blue light-induced damage to retinal pigment epithelial cells by inhibiting FGF2 expression.","authors":"Guang-Ming Liu, Yan Liu","doi":"10.1007/s10616-025-00752-4","DOIUrl":"https://doi.org/10.1007/s10616-025-00752-4","url":null,"abstract":"Age-related macular degeneration (AMD) is a debilitating retinal disorder that may lead to progressive vision loss. One contributing factor to AMD pathogenesis is excessive blue light (BL) exposure. In this study, we investigated the therapeutic potential of exosomes derived from human umbilical cord blood mesenchymal stem cells (hUCMSC-EXs) in addressing BL-induced damage to ARPE-19 human retinal pigment epithelial (RPE) cells and explored the underlying mechanisms. Our findings revealed that BL exposure induced morphological alterations in ARPE-19 cells, accompanied by a time-dependent decline in cell viability, increased apoptosis, heightened oxidative stress, and inflammatory responses; however, hUCMSC-EXs dose-dependently mitigated BL-induced ARPE-19 cell damage. Interestingly, hUCMSC-EXs were found to suppress the upregulation of fibroblast growth factor 2 (FGF2) in BL-exposed ARPE-19 cells. Furthermore, FGF2 overexpression partially counteracted the inhibitory effects of hUCMSC-EXs on FGF2 expression and compromised the protective benefits of hUCMSC-EXs against BL-induced ARPE-19 cell damage. In conclusion, our results suggest that hUCMSC-EXs shield ARPE-19 cells from BL-induced harm by inhibiting FGF2 expression.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"88"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970020","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}

引用次数: 0

Mechanism of the N6-methyladenosine reader heterogeneous nuclear ribonucleoprotein C facilitating immune escape in thyroid cancer by stabilizing programmed death ligand 1. n6 -甲基腺苷解读器异质核核糖核蛋白C通过稳定程序性死亡配体促进甲状腺癌免疫逃逸的机制

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-05-06 DOI: 10.1007/s10616-025-00755-1

Nuoxuan Li, Liang Wang, Jie Yao, Hong Yang

{"title":"Mechanism of the N6-methyladenosine reader heterogeneous nuclear ribonucleoprotein C facilitating immune escape in thyroid cancer by stabilizing programmed death ligand 1.","authors":"Nuoxuan Li, Liang Wang, Jie Yao, Hong Yang","doi":"10.1007/s10616-025-00755-1","DOIUrl":"https://doi.org/10.1007/s10616-025-00755-1","url":null,"abstract":"Thyroid cancer (TC) is a leading malignancy of the endocrine system. We investigated mechanism of the N6-methyladenosine (m6A) reader heterogeneous nuclear ribonucleoprotein C (HNRNPC) facilitating immune escape in TC by stabilizing programmed death ligand 1 (PD-L1). HNRNPC expression in TC tissues was analyzed using databases. Human TC cells (BHT-101, B-CPAP, SW579) and human thyroid follicular epithelial cells (Nthy-ori3-1) were cultured in vitro. SW579 cells were treated with pcDNA3.1-HNRNPC (oe-HNRNPC) and small interfering (si)-PD-L1, and B-CPAP cells were transfected with si-HNRNPC. HNRNPC and PD-L1 expression levels were assessed by RT-qPCR and Western blot. Cell proliferation, migration and invasion were evaluated by CCK-8, colony formation, and Transwell assays. Carboxyfluorescein diacetate succinimidyl ester-labelled CD8+ T cell proliferation and effector cytokine (interferon-γ, tumor necrosis factor-α) levels were measured by flow cytometry and ELISA. The correlation between HNRNPC and PD-L1 expression in TC tissues, m6A modification sites on PD-L1 messenger RNA (mRNA), and HNRNPC-PD-L1 interaction were analyzed by databases and RIP assay. PD-L1 m6A modification was determined by Me-RIP assay. PD-L1 mRNA stability was detected by treating cells with actinomycin D. HNRNPC was notably highly expressed in TC cells. HNRNPC promoted TC cell proliferation, migration and invasion, facilitating immune escape. Mechanistically, HNRNPC mediated m6A modification to strengthen PD-L1 mRNA stability and up-regulate PD-L1 expression. Moreover, knockdown of PD-L1 partially reversed the promotional effect of HNRNPC on immune escape in TC cells. HNRNPC bolstered PD-L1 stability and up-regulated PD-L1 expression through m6A modification, thus promoting immune escape in TC.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"96"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978502","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}

引用次数: 0

Correction: PABPC1 silencing inhibits pancreatic cancer cell proliferation and EMT, and induces apoptosis via PI3K/AKT pathway. 修正：PABPC1沉默抑制胰腺癌细胞增殖和EMT，并通过PI3K/AKT通路诱导细胞凋亡。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-05-13 DOI: 10.1007/s10616-025-00760-4

Changren Zhu, Cuimei Wang, Xiaodong Wang, Shuangshuang Dong, Qing Xu, Jun Zheng

引用次数: 0

Metformin inhibits subretinal fibrosis by activating Klotho by miR-126-5p. 二甲双胍通过miR-126-5p激活Klotho抑制视网膜下纤维化。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-04-02 DOI: 10.1007/s10616-025-00744-4

Zhijuan Hua, Qin Zhu, Jingfei Yang, Yuxiang Zheng, Wenchang Yang, Dongli Li, Yixin Cui, Lu Shen, Lingna Rao, Xiaofan Zhang, Ling Yuan

{"title":"Metformin inhibits subretinal fibrosis by activating Klotho by miR-126-5p.","authors":"Zhijuan Hua, Qin Zhu, Jingfei Yang, Yuxiang Zheng, Wenchang Yang, Dongli Li, Yixin Cui, Lu Shen, Lingna Rao, Xiaofan Zhang, Ling Yuan","doi":"10.1007/s10616-025-00744-4","DOIUrl":"10.1007/s10616-025-00744-4","url":null,"abstract":"Subretinal fibrosis is a main cause of visual loss in patients with neovascular age-related macular degeneration (nAMD), for whom there has been a lack of effective medication. Metformin can improve inflammation and angiogenesis in eye diseases. This study aimed to investigate the mechanism by which metformin inhibits subretinal fibrosis. A subretinal fibrosis cell model was induced by treating human retinal pigment epithelial cells (ARPE-19) with TGF-β1, a subretinal fibrosis mouse model was induced by a laser, and both cells and mice were treated with metformin. Cell proliferation, migration, and invasion were detected by CCK-8, scratch, and Transwell assays. Western blotting and immunofluorescence were used to evaluate protein expression levels, and RT‒qPCR was used to detect gene expression levels. HE and Masson staining were used to observe the morphological changes in retinal and choroidal tissues. Metformin treatment inhibited the TGF-β1-induced proliferation, migration, invasion and epithelial‒mesenchymal transition (EMT) of ARPE-19 cells and effectively ameliorated laser-induced subretinal fibrosis in mice. Mechanistically, metformin inhibits the expression of miR-126-5p, promotes Klotho synthesis, slows the progression of subretinal fibrosis, and miR-126-5p targets and negatively regulates Klotho. Metformin activates Klotho by inhibiting miR-126-5p, thereby reversing TGF-β1-induced ARPE-19 cell EMT and improving laser-induced subretinal fibrosis in mice.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"84"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794889","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}

引用次数: 0

Blocking circular RNA FNDC3B induces fibroblast-like synoviocytes dysfunction to ameliorate rheumatoid arthritis through regulating the miR-125a-5p-Hexokinase2 axis. 阻断环状RNA FNDC3B诱导成纤维细胞样滑膜细胞功能障碍，通过调节miR-125a-5p-Hexokinase2轴改善类风湿关节炎。

IF 2 4区生物学

Cytotechnology Pub Date : 2025-06-01 Epub Date: 2025-03-26 DOI: 10.1007/s10616-025-00745-3

Jiaxin Fu, Zhi Liu, Guangxin Zhang, Chun Zhang

{"title":"Blocking circular RNA FNDC3B induces fibroblast-like synoviocytes dysfunction to ameliorate rheumatoid arthritis through regulating the miR-125a-5p-Hexokinase2 axis.","authors":"Jiaxin Fu, Zhi Liu, Guangxin Zhang, Chun Zhang","doi":"10.1007/s10616-025-00745-3","DOIUrl":"10.1007/s10616-025-00745-3","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune inflammatory joint disease. The cause of synovitis in rheumatoid arthritis involves the interaction between immune cells/macrophages and fibroblast-like synoviocytes (FLSs-RA). The impact of circular RNAs on FLSs and their role in RA pathology is still unknown. This study aimed to investigate the roles and molecular mechanisms of circular RNA FNDC3B in regulating cell injury and glucose metabolism of FLSs in RA. We demonstrated that circFNDC3B was significantly upregulated and miR-125a-5p was significantly downregulated in FLSs from RA patients. When circFNDC3B was silenced or miR-125a-5p was overexpressed, it reduced FLSs-RA glucose metabolism and increased oxidative stress-induced cell injury. Through bioinformatics analysis, RNA pull-down, and luciferase assays, it was found that circFNDC3B sponged miR-125a-5p to create a ceRNA network in FLSs-RA. The glucose metabolism rate was elevated in FLSs-RA, showing a glucose-dependent characteristic compared to normal FLSs. The enzyme hexokinase 2 (HK2), which is crucial for glucose metabolism, was identified as a direct target of miR-125a-5p in FLSs. In rescue experiments, restoring miR-125a-5p in circFNDC3B-overexpressing FLSs-RA successfully counteracted the circFNDC3B-promoted glucose metabolism and resistance to cell injury. In conclusion, this study highlighted the important roles and molecular mechanisms of circFNDC3B in accelerating glucose metabolism and preventing cell apoptosis in fibroblast-like synoviocytes during rheumatoid arthritis by modulating the miR-125a-5p-HK2 axis. Targeting the circFNDC3B-mediated glucose metabolism pathway could be a promising strategy for rheumatoid arthritis therapy.Supplementary information: The online version contains supplementary material available at 10.1007/s10616-025-00745-3.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"83"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11947371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751456","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}

引用次数: 0