Cytotechnology最新文献

{"title":"The applications of organoids in kidney diseases: progress and challenges.","authors":"Qianying Feng, Junzheng Yang","doi":"10.1007/s10616-026-01064-x","DOIUrl":"10.1007/s10616-026-01064-x","url":null,"abstract":"<p><p>Kidney organoids are a type of three-dimensional cellular aggregates derived from primary tissues or stem cells cultured in vitro. Under specific induction conditions, these cell aggregates can differentiate into complex renal nephron structures, including glomeruli, proximal tubules, and distal tubules. These cells have been demonstrated to possess a remarkable capacity for self-renewal and self-organization, demonstrating a high degree of structural and functional similarity to the structure of kidney organs and the certain renal functions. Due to their ability to replicate the key renal structures and functions, they hold significant potential in various areas of kidney disease research, including novel drug development, disease modeling, personalized medicine, and therapeutic interventions for kidney diseases. In this review, we summarize the recent advancements in organoid culture technology and the applications of organoids in kidney diseases. The technical challenges and current limitations of organoid technology and possible solutions are also discussed. The aim of this review is to promote the development of organoid technology and to provide the theoretical knowledge for researchers in related fields.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"194"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13546199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900108","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":"Hydroxysafflor yellow A attenuates TBHP-induced lipid peroxidation and calcification-related changes in human endplate chondrocytes: involvement of SLC7A11/GPX4 signaling.","authors":"Zongyu Zhang, Peng Zhang, Zhijing Zhou, Xuefeng Li, Yongfeng Huo","doi":"10.1007/s10616-026-01060-1","DOIUrl":"10.1007/s10616-026-01060-1","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is a chronic degenerative disorder, with oxidative stress being one of the primary driving mechanisms of IDD. Hydroxysafflor yellow A (HSYA), a major active component of safflower, exhibits potent antioxidant, anti-inflammatory, and anti-apoptotic properties. However, its role in IDD remains unclear. To explore the mechanism underlying HSYA's protection against tert-butyl hydroperoxide (TBHP)-induced oxidative stress in chondrocytes. Chondrocytes were treated with TBHP (100 µM) to establish an oxidative stress model, followed by administration of HSYA (5, 10, and 20 µM). Cell viability and apoptosis were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Lipid peroxidation levels were evaluated by immunofluorescence. The protein expression levels of solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), SRY-box transcription factor 9 (SOX9), type II collagen (COL2), matrix metalloproteinase 3 (MMP-3), type X collagen (COL10), and runt-related transcription factor 2 (RUNX2) were analyzed by western blot analysis. mRNA expression of SLC7A11, GPX4, COL10, and RUNX2 was determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Calcium deposition in endplate chondrocytes was examined by Alizarin Red staining. Compared with the control group, treatment with TBHP markedly reduced chondrocyte viability, promoted ferroptosis, and significantly elevated intracellular lipid peroxidation levels. Furthermore, TBHP exposure triggered a prominent increase in chondrocyte apoptosis, cartilage endplate (CEP) degeneration, and chondrocyte calcification. Notably, all these findings were dose-dependently reversed by HSYA intervention. However, SLC7A11 knockdown abolished the protective effects of HSYA against TBHP-induced chondrocyte damage. In summary, our findings indicate that HSYA protects chondrocytes from TBHP-induced oxidative stress, ferroptosis, apoptosis, and calcification, and alleviates CEP degeneration, at least partly associated with SLC7A11/GPX4-related redox regulation, providing in vitro experimental evidence for exploring its value in IDD-related research.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"195"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13546277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900162","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":"Decoding chromosomal instability in neutrophil signature in the pathogenesis of periodontitis: evidence from artificial intelligence-driven multi-omics and in vitro validation.","authors":"Bichu Zhang, Shixin Yao, Zhang Zhang, Feng Yi","doi":"10.1007/s10616-026-01046-z","DOIUrl":"10.1007/s10616-026-01046-z","url":null,"abstract":"<p><p>Periodontitis (PDT) is a chronic inflammatory disease driven by a dysregulated host immune response, with neutrophils playing a pivotal role. Chromosomal instability (CI) has emerged as a potent trigger of inflammation, yet its involvement in non-malignant diseases like PDT remains unexplored. Bulk RNA-seq data from gingival tissues between PDT patients and healthy control(HC) were analyzed via Limma framework to identify differentially expressed genes (DEGs) and CI-associated DEGs. WGCNA pinpointed a module correlated with neutrophil infiltration. Next, CI and neutrophil(CIN)-associated signature were acquired by integrating Limma and WGCNA results. NMF was used for molecular subtyping based on CIN-associated signature. A machine learning framework constructed a diagnostic model, with SHAP analysis identifying the hub gene based on PDT training and validation bulk profiles. Single-cell RNA-seq data validated cellular-level findings, and cutting-edge analytical framework inferred TFF3 functional impact at neutrophil of PDT patients in a temporal and spatial manners. The AI platform DrugReflector screened for therapeutic compounds for PDT patients, and in vitro assays examined the expression of hub gene. We identified 5 CI and neutrophil(CIN)-associated signature for PDT patients, which can guide the forecasting of PDT pathogenesis and PDT patient stratification. Besides, TFF3 can be considered as CIN-associated up-regulated pathogenic factor involved in PDT pathogenesis, which was mainly expressed in neutrophil. BRD-K92455082 as a candidate therapeutic agent targeting TFF3 for the treatment of PDT. This study first identifies a novel CIN-associated co-expression patterns in PDT. TFF3 can be considered as a candidate hub gene associated with a pro-inflammatory neutrophil state, providing new insights into the molecular taxonomy of PDT.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"188"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863855","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":"Mitochondrial Peptide SHLP2 Limits Poly(I: C)-Induced Alveolar Epithelial Injury by Modulating Redox, Apoptotic, Inflammatory, and Inflammasome Responses.","authors":"Sara Betül Ramazan, Bedircan Turan, Aysegul Turkkol, Şerife Gökçe Çalişkan, Merve Ece Oyur, Muhammed Hasan Alici, Umut Kerem Kolac","doi":"10.1007/s10616-026-01070-z","DOIUrl":"10.1007/s10616-026-01070-z","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Type II alveolar epithelial (ATII) cells play a central role in pulmonary homeostasis, epithelial repair, and innate antiviral defense. Polyinosinic: polycytidylic acid [Poly(I: C)], a synthetic analog of viral double-stranded RNA, induces a viral-like epithelial injury phenotype characterized by oxidative stress, mitochondrial dysfunction, inflammation, and inflammasome-associated responses. Small humanin-like peptide 2 (SHLP2), a mitochondrial-derived peptide, has been associated with cytoprotective and mitochondrial regulatory effects; however, its role in viral-like alveolar epithelial injury remains unclear. This study investigated the effects of SHLP2 on Poly(I: C)-induced cellular damage in human ATII cells. Human ATII cells were assigned to four groups: control, SHLP2 alone, Poly(I: C) alone, and subsequent SHLP2 treatment during continued Poly(I: C) exposure. Cell viability was assessed by MTT assay. Apoptosis was evaluated by Annexin V-FITC/PI flow cytometry and by measuring &lt;i&gt;BCL2/BAX&lt;/i&gt; expression. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) production were analyzed. Oxidative stress-related markers, inflammatory mediators and antiviral response-associated markers, and inflammasome-associated molecules were evaluated by qPCR and ELISA. In silico protein-peptide docking was performed to predict possible interactions with SHLP2. Poly(I: C) reduced cell viability and promoted apoptosis, mitochondrial depolarization, and ROS accumulation in human ATII cells. These effects were accompanied by altered &lt;i&gt;BCL2/BAX&lt;/i&gt; expression, increased &lt;i&gt;SOD2&lt;/i&gt; and &lt;i&gt;GPX1&lt;/i&gt; expression, changes in total NRF2 and KEAP1 protein levels, elevated inflammatory mediators and Poly(I: C)-induced antiviral response-associated markers, including TNF-α, IL-6, NF-κB, TICAM1, and IFN-β, and increases in NLRP3 inflammasome-associated markers, including NLRP3, cleaved caspase-1, IL-1β, and IL-18. SHLP2 alone did not exert cytotoxic effects. Notably, subsequent SHLP2 treatment during continued Poly(I: C) exposure attenuated apoptosis, mitochondrial depolarization, ROS accumulation, inflammatory mediator production, TICAM1 and IFN-β levels, and several inflammasome-associated markers and outputs. Docking analyses predicted possible interactions of SHLP2 with TICAM1 and KEAP1, providing hypothesis-generating in silico evidence for potential associations with inflammatory and redox-related proteins. SHLP2 treatment was associated with reduced mitochondrial depolarization, oxidative stress, and apoptosis, together with changes in inflammatory and antiviral response-associated markers and NLRP3 inflammasome-related outputs in Poly(I: C)-exposed human ATII cells. These findings identify SHLP2 as an early-stage candidate for further investigation in Poly(I: C)-induced viral-like alveolar epithelial injury.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Supplementary information: &lt;/strong&gt;The online version contains supplementary material available at https://d","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"200"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024046","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":"Unraveling berberine's multi-target mechanism in combating early-stage masld: a network pharmacology and in vitro study.","authors":"Shenglong Wei, Huajie He, Yong Xie, Youhua Wang, Xiaojiang Zhou","doi":"10.1007/s10616-026-01057-w","DOIUrl":"10.1007/s10616-026-01057-w","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a global health burden with limited therapies. Berberine (BBR) shows promise against MASLD, but its molecular mechanisms remain unclear. Network pharmacology predicted BBR-MASLD intersecting targets, followed by protein-protein interaction (PPI) network construction, GO/KEGG enrichment, and molecular docking. In vitro validation used FFA-induced HepG2 steatosis cells with Oil Red O staining, triglyceride assay, RT-qPCR, and Western blot for p-AKT/AKT. From 147 intersecting targets, six functional core targets were identified: AKT1, IL6, TP53, TNF, IL1B, and BCL2. Enrichment analyses implicated insulin resistance, lipid metabolism, and inflammation. Molecular docking confirmed strong BBR-core protein binding. In vitro, BBR dose-dependently reduced lipid accumulation and triglyceride levels, downregulated lipogenic (SREBP-1c) and pro-inflammatory (IL-6, IL-1β, TNF-α) genes, and restored insulin signaling (AKT1) and apoptosis-related (TP53) gene expression.BBR increased the p-AKT (Ser473)/total AKT ratio as shown by Western blot. BBR attenuates lipid accumulation and partially reverses steatosis-related transcriptional changes in an FFA-induced HepG2 model, including restoration of AKT1 signaling at both mRNA and protein phosphorylation levels. These findings suggest that BBR exerts protective effects againstearly hepatocellular steatosist hrough coordinated regulation of lipid metabolism, inflammation, and stress-related targets. This study provides a network-based rationale for further in vivo and mechanistic investigation in MASLD, and identifies potential pharmacodynamic biomarkers for future clinical trials.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01057-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"192"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896702","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":"Engeletin alleviates MSU-induced inflammatory and tubular injury in vitro by targeting TLR4 and NFKB1.","authors":"Ruiwei Han, Chuanchao Wu, Xiaofeng Liang, Xiaoxue Xiang, Jiayi Wang, Jianhui Jiang, Qiuxia Lin, Li He","doi":"10.1007/s10616-026-01047-y","DOIUrl":"10.1007/s10616-026-01047-y","url":null,"abstract":"<p><p>The possible mechanisms of engeletin in hyperuricemic nephropathy (HN) has remained obscured; consequently, this investigation seeks to illuminate both the therapeutic potential and the mechanistic underpinnings of engeletin within the context of HN in vitro. The anti-HN mechanisms of engeletin were evaluated through in silico target identification and network pharmacology methodologies. Molecular docking was conducted using AutoDock Vina. RAW 264.7 macrophages and HK‑2 renal epithelial cells were treated with engeletin with or without monosodium urate (MSU) stimulation. Cell viability was assessed by the CCK‑8 assay. Migration was evaluated using Transwell assays. Pro‑inflammatory cytokines were measured by ELISA. In HK‑2 cells, mRNA levels of URAT1, GLUT9, OAT1, and ABCG2 were determined by qRT‑PCR, and XOD activity was measured using a commercial kit. TLR4 or NFKB1 overexpression was performed to confirm pathway involvement. TLR4 and NFKB1 were identified to be key targets for engeletin against HN. Molecular docking revealed stable binding of engeletin to TLR4 (‑6.6 kcal/mol) and NFKB1 (‑7.1 kcal/mol) with hydrogen bonds and anion pi interactions. Engeletin at 50 and 100 µM showed no cytotoxicity and significantly suppressed MSU‑induced RAW 264.7 cell migration and secretion of TNF‑α, IL‑6, IL‑1β, and MCP‑1. In HK‑2 cells, engeletin (100 µM) downregulated urate reabsorption transporters URAT1 and GLUT9, upregulated excretion transporters OAT1 and ABCG2, and inhibited XOD activity. Overexpression of TLR4 or NFKB1 markedly reversed all these effects. Engeletin can suppress cytokine release and macrophage migration, enhance renal urate excretion, and inhibite XOD activity in vitro, partly by targeting TLR4 and NFKB1.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01047-y.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"184"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817795","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":"BACH2 ameliorates lung injury in LPS-induced sepsis through activation of Nrf2 signaling.","authors":"Lihui Wang, Xiaoliang Ji, Shimin Dong, Qinglong Lu","doi":"10.1007/s10616-026-01024-5","DOIUrl":"10.1007/s10616-026-01024-5","url":null,"abstract":"<p><p>To explore the function and molecular mechanism of BACH2 in septic lung injury induced by lipopolysaccharide (LPS). We established LPS-induced septic lung injury models in mice and human bronchial epithelial BEAS-2B cells. By overexpressing/knocking down BACH2 and knocking down Nrf2, combined with pathological staining, molecular biology and cell experiment techniques, we detected the levels of lung tissue injury, inflammation and pulmonary fibrosis, and verified the regulatory relationship between BACH2 and Nrf2. In the lung tissues of mice with LPS-induced septic lung injury, the expression level of BACH2 was decreased in a time-dependent pattern. Overexpression of BACH2 significantly alleviated LPS-induced pathological injury of mouse lung tissues, inhibited neutrophil infiltration, and reduced the release of inflammatory cytokines and the degree of pulmonary fibrosis. BACH2 could directly bind to the -2000 ~ -1800 bp region of the Nrf2 promoter and upregulate its expression, and knockdown of Nrf2 completely reversed the lung protective effect of BACH2. BACH2 exerts anti-inflammatory and anti-fibrotic effects by directly binding to and activating the Nrf2 signaling pathway, thereby ameliorating LPS-induced septic lung injury. The BACH2/Nrf2 axis may serve as a candidate molecular target for further preclinical research on septic lung injury treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01024-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"190"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863816","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":"Nano guar gum triphenyl phosphonium conjugated rutin complex ameliorates hypertrophy in H9c2 cells via mitochondrial-mediated pathways.","authors":"R S Soumya, M S Ajay Krishna, Genu George, B S Sasidhar, K G Raghu","doi":"10.1007/s10616-026-01045-0","DOIUrl":"10.1007/s10616-026-01045-0","url":null,"abstract":"<p><p>Mitochondria-targeted antioxidants have emerged as a promising frontier in drug discovery, offering advantages over conventional antioxidants owing to recent technological advances. As the primary intracellular source of reactive oxygen species (ROS) mitochondria play a critical role in cellular health. Consequently, excessive mitochondrial ROS generation is heavily implicated in the pathogenesis of cardiovascular, neurodegenerative, and metabolic disorders. The etiopathogenesis of cardiovascular disease is mainly due to the dysfunction of mitochondria. Therefore, mitochondrial dysfunction is a novel curious target for developing new drug therapies. In this study, mitochondrial antioxidant (Ru-TPP-GGN) was prepared by incorporating triphenylphosphonium (TPP) conjugated rutin into guar gum nanoparticles (GGN) and was evaluated against angiotensin II (Ang II) induced hypertrophy in the H9c2 cell lines. The size of the synthesized Ru-TPP-GGN was about ≈ 15 nm, and it was subjected to detailed characterization to confirm its nano-characteristics. The cytoxicity analysis showed that the Ru-TPP-GGN was nontoxic to the cells. The cells treated with Ang II showed abnormalities in mitochondria with surplus superoxide generation, an increase in atrial natriuretic peptide (ANP) (125.75%↑) and brain natriuretic peptide (BNP) (82.75%↑) level, dissipation of mitochondrial transmembrane potential (ΔΨm), mitochondrial permeability transition pore (mPTP) opening, upregulation of transforming growth factor-β (TGF-β) protein expression, and alterations in the expression of proteins (OPA1, MFN1/2, FIS1, DRP1, and MFF) involved in mitochondrial biogenesis. Ru-TPP-GGN was found to avert the progression of hypertrophy via safeguarding mitochondrial integrity and dynamics. It is found to be a potential nanomaterial for further exploration for the development of mitochondrial antioxidant-based therapies against cardiac hypertrophy.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 5","pages":"189"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863904","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":"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}