Cytotechnology最新文献

{"title":"LncRNA MIR503HG promotes delayed fracture healing by regulating the miR-497-5p/HMGA2 axis.","authors":"Yiwei Li, Borui Zhang, Mingdong Zhang, Zheng Li, Bin Wang","doi":"10.1007/s10616-026-00942-8","DOIUrl":"https://doi.org/10.1007/s10616-026-00942-8","url":null,"abstract":"<p><p>Delayed fracture healing (DFH) frequently occurs as a complication following a fracture. Most fractures heal successfully after surgery, but 5%-10% of patients experience delayed or non-healing, causing pain, disability, psychological issues, and economic burdens. This study aims to investigate the abnormal expression and clinical role of MIR503HG in DFH, as well as to explore the molecular mechanism by which MIR503HG affects fracture healing. This study included a cohort of 187 fracture patients, comprising 90 normal healing individuals and 97 delayed healing patients. The expression levels of MIR503HG in both serum and cellular samples were quantified utilizing RT-qPCR. The predictive capacity of MIR503HG for DFH was assessed through the construction of a ROC curve. The impact of MIR503HG on osteoclast proliferation was examined via the CCK-8 assay, while the levels of apoptosis were determined by means of flow cytometry. MIR503HG expression was elevated in the serum of DFH patients, and this heightened expression may serve as a predictive biomarker for the onset of DFH. Suppression of MIR503HG expression inhibited the proliferation and differentiation of osteoclasts while concurrently promoting cellular apoptosis. Inhibition of miR-497-5p was found to counteract the effects of MIR503HG knockdown on osteoclast proliferation, apoptosis, and differentiation markers. Moreover, MIR503HG enhances the expression of HMGA2 by directly inhibiting the expression of miR-497-5p. MIR503HG may delay fracture healing by regulating the miR-497-5p/HMGA2 axis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00942-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"78"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13050351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627436","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":"Skin-whitening, antioxidant, and anti-inflammatory effects of <i>Angelica decursiva</i> ethanol extract.","authors":"Jusuk Hwang, Si Eun Yoon, Sohee Moon, Hyeon Jin Kim, Jae Youl Cho","doi":"10.1007/s10616-026-00961-5","DOIUrl":"https://doi.org/10.1007/s10616-026-00961-5","url":null,"abstract":"<p><p>The multifunctional potential of <i>Angelica decursiva</i> ethanol extract (Ad-EE) was evaluated to address the safety and efficacy limitations of conventional whitening agents. Experimental results indicate that Ad-EE suppresses melanin secretion in B16F10 cells in a dose-dependent manner. Furthermore, under 20 mJ/cm2 UVB irradiation, Ad-EE reduces the mRNA and protein expression levels of Tyrosinase and TRP1, thereby mitigating both hormonal and environmental triggers. Comprehensive chemical profiling using gas chromatography-mass spectrometry (GC-MS) and high-resolution liquid chromatography-mass spectrometry (HR- LC-MS) revealed a complex phytochemical matrix extending beyond simple volatile compounds. Molecular docking analysis demonstrated that key metabolites, including 1- methylinosine and adhyperforin, possess high binding affinities for the TRP1 catalytic pocket. Ad-EE also exhibits significant antioxidant and anti-inflammatory activities. Multiple assays, including ABTS and FRAP, showed a dose-dependent increase in radical scavenging and ferric-reducing capacities. In HaCaT and RAW264.7 cells, Ad-EE improved cellular redox status by upregulating endogenous antioxidant genes, including HO-1 and NQO-1, while suppressing inflammatory mediators. By simultaneously inhibiting key enzymatic pathways and enhancing cellular defense signaling, Ad-EE disrupts melanogenesis in response to diverse stimuli. These findings provide a strong molecular basis for considering Ad-EE as a versatile, natural candidate for advanced cosmeceutical applications.</p><p><strong>Graphical abstract: </strong><i>Angelica decursiva</i> ethanol extract (Ad-EE) reduces melanin production showing suppression of tyrosinase, TRP1, and TRP2, induces the expression of anti-oxidative genes such as HO-1, and inhibits LPS-induced inflammatory response via down-regulation of Src activity.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"99"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812099","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":"MIR99AHG alleviates reflux esophagitis caused by gastroesophageal reflux disease by downregulating miR-200a-3p.","authors":"Jincai Chen, Qianli Liu, Xiaowen Zheng, Xiaoxin Wang, Fanyu Wu, Chunlei Li, Limin Tong","doi":"10.1007/s10616-026-00980-2","DOIUrl":"https://doi.org/10.1007/s10616-026-00980-2","url":null,"abstract":"<p><p>Reflux esophagitis (RE) can progress to severe complications if not diagnosed and treated promptly. MIR99AHG is downregulated in the precursor disease of RE. This study aims to investigate the expression and regulatory mechanisms of MIR99AHG in RE. This study included 176 patients with RE. RT-qPCR was used to detect the expression of MIR99AHG, miR-200a-3p, Bax, Bcl-2, and caspase-3 For cellular experiments: cell proliferation, apoptosis, and the levels of inflammatory cytokines in cell culture supernatants were assessed using CCK-8 assay, Annexin V-FITC/PI double staining, and ELISA, respectively. DLR validated the binding between MIR99AHG and miR-200a-3p. ROC analysis evaluated their diagnostic value. Pearson correlation analysis assessed their relationship. In the RE and cell model groups, MIR99AHG expression was downregulated while miR-200a-3p expression was upregulated. MIR99AHG targeted and bound miR-200a-3p, negatively regulating its expression. Both demonstrated significant diagnostic value. Following modeling with acid salts and bile salts, cellular proliferation capacity decreased, apoptosis rates increased, and inflammatory factor levels rose. Upon overexpression of MIR99AHG, miR-200a-3p expression levels were downregulated, leading to enhanced cellular proliferation capacity, reduced apoptosis rates, and decreased inflammatory factor levels. MIR99AHG represents a promising clinical biomarker in RE. By downregulating miR-200a-3p levels, MIR99AHG may promote proliferation and repair of esophageal mucosal epithelial cells, inhibit excessive apoptosis, and mitigate local inflammatory responses, thereby exerting multifaceted protective effects during RE progression.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"102"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834666","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":"20(S)-Ginsenoside Rg3 suppresses lung cancer-associated fibroblast activation associated with IL-17RD-FGF-MAP2K4-JNK signaling.","authors":"Xinyu Zhang, Lei Xia, Feng Cheng, Jihong Zhuang, Ruiying Rao, Jiaqi Meng, Jinhe Xu, Wenting Zhang, Zongyang Yu","doi":"10.1007/s10616-026-00957-1","DOIUrl":"https://doi.org/10.1007/s10616-026-00957-1","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) are key components of the tumor microenvironment (TME) that contribute to tumor progression and therapeutic resistance in non-small cell lung cancer (NSCLC). However, effective strategies targeting CAF regulation remain limited. Here, we investigated the effects of the plant-derived compound 20(S)-Ginsenoside Rg3 on CAFs using an integrated network pharmacology and experimental validation approach. Network pharmacology analysis identified 107 overlapping targets between Rg3 and NSCLC. PPI network analysis highlighted EGFR, JUN, TP53, and STAT3 as key hub genes. KEGG enrichment analysis indicated that these targets were significantly enriched in the IL-17 and MAPK signaling pathways. These genes and pathways have been associated with fibroblast activation and tumor stromal remodeling, suggesting a potential role of Rg3 in regulating CAF-related processes within the tumor microenvironment. Functional experiments demonstrated that Rg3 inhibited CAF proliferation, colony formation and migration, while inducing apoptosis and mitochondrial dysfunction. Mechanistically, Rg3 upregulated IL-17RD and suppressed FGFR1-MAP2K4-JNK-c-Jun signaling. Furthermore, co-culture experiments revealed that Rg3-treated CAFs exhibited reduced pro-tumorigenic effects on NSCLC cells, indicating impaired tumor-stroma communication. Collectively, these findings demonstrate that 20(S)-Ginsenoside Rg3 suppresses CAF activation and function associated with the IL-17RD-FGF-MAP2K4-JNK-c-Jun signaling pathway, highlighting its potential as a tumor microenvironment-targeted therapeutic agent in NSCLC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00957-1.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"79"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638158","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":"Repair of rat skin defects using decellularized skin matrix/chitosan hybrid hydrogels.","authors":"Chen Wu, Yunjie Wang, Chao Ci, Chen Liu","doi":"10.1007/s10616-026-00954-4","DOIUrl":"https://doi.org/10.1007/s10616-026-00954-4","url":null,"abstract":"<p><p>Full-thickness skin wounds pose a substantial clinical challenge and burden in the medical field. Currently, skin tissue engineering is a promising approach with broad potential applications in the treatment of skin defects. Decellularized skin matrix (DSM) have been extensively utilized as scaffolds in skin tissue engineering because of their complex spatial organization and ability to facilitate the attachment of cells that secrete active cytokines. Herein, DSM/chitosan hybrid hydrogels with different DSM:chitosan ratios (DSM/Chitosan-1, 8:2; DSM/Chitosan-2, 5:5; and DSM/Chitosan-3, 2:8) were prepared with the crosslinker genipin. Rat adipose-derived stem cells (ADSCs) were seeded onto the hybrid hydrogels. Cytoskeleton staining indicated that rat ADSCs thrived on the three hybrid hydrogels. Among the hybrid hydrogels, ADSCs seeded onto DSM/Chitosan-1 exhibited the greatest gene expression levels of cytokeratin-10, cytokeratin-14, and involucrin, and the lowest expression of interleukin-6. Furthermore, according to hematoxylin and eosin staining, DSM/Chitosan-1 exhibited excellent repair ability for full-thickness skin defects in rats. Overall, the DSM/Chitosan-1 hybrid hydrogel exhibits substantial promise as an alternative means for the repair of cutaneous lesions in skin tissue engineering.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"97"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812093","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":"Evaluation of the impact of glycolysis-related gene signatures on prognosis and therapeutic targeting in lung adenocarcinoma.","authors":"Yalan Tang, Jundan Xiao, Xiaowei Zhong, Zhigang Chen","doi":"10.1007/s10616-026-00953-5","DOIUrl":"https://doi.org/10.1007/s10616-026-00953-5","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Abnormal glycolysis is one of the hallmarks of cancer and plays a significant role in its progression. This study investigates the association between glycolysis genes and the progression of lung adenocarcinoma (LUAD). Utilizing various bioinformatics techniques, the research explores the heterogeneity of glycolysis genes in different LUAD cell types, identifies glycolysis-related prognostic signatures (GRPS). We obtained one training set for model construction from the Cancer Genome Atlas (TCGA) database, and also obtained four LUAD gene expression datasets as validation sets from the Gene Expression Omnibus (GEO) database. The single-cell RNA sequencing (scRNA seq) data also comes from the GEO database. Firstly, the \"limma\" R package was used to identify differentially expressed glycolysis related genes, and a machine learning computational framework composed of multiple combinations was used to preliminarily screen for glycolysis related prognostic markers (GRPS) in LUAD. Based on these GRPS, prognostic features were developed and validated through survival analysis, column chart development, and ROC curve analysis. The ssGSEA algorithm, ESTIMATE algorithm, and seven integrated computational algorithms from the TIMER 2.0 database were used to analyze the immune cell infiltration patterns of different risk groups. Analyze scRNA seq data to evaluate the distribution of GRPS and intercellular communication among various cell types, and further determine the core GRPS through the \"hdWGCNA\" and \"ConstructNetwork\" packages. In addition, we also evaluated the responsiveness of high and low-risk groups to 198 drugs using the \"OncoPredict\" software package. Result: We found that the glycolytic activity score of tumor tissue was significantly higher than that of normal tissue, and a total of 49 upregulated genes and 15 downregulated genes were selected from the total. Based on a machine learning computational framework, a total of 8 GRPS were screened, which constitute the prognostic features of LUAD patients. This feature demonstrates strong prognostic value, as confirmed by univariate and multivariate Cox regression analysis. Significant differences in tumor microenvironment (TME) immune infiltration were observed between high and low-risk groups. ScRNA seq revealed the distribution and expression of cell type specific GRPS, particularly in T cells, epithelial cells, and fibroblasts, while also revealing the strong cell-cell communication ability of the high GRPS group. The hdWGCNA analysis ultimately identified five core GRPS, namely DDIT4, FKBP4, CHPF, EFNA3, and B3GNT3. In addition, there are significant differences in sensitivity to most drugs between high-risk and low-risk cohorts, with WIKI4 and Lapatinib negatively correlated with risk scores, while Doramapimod and Niraparib positively correlated with risk scores. This study established a GRPS based risk feature for LUAD, demonstrating strong predictive power for prognosis assessment. The","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"88"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688569","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":"Liquid-liquid phase separation of TRIM21 regulates EZH2-mediated ferroptosis to facilitate hepatocellular carcinoma progression.","authors":"Li Xu, Shilun Wu, Changyu Yao, Shaohong Wang, Surgery","doi":"10.1007/s10616-026-00968-y","DOIUrl":"https://doi.org/10.1007/s10616-026-00968-y","url":null,"abstract":"<p><p><i>Background</i> Liquid-liquid phase separation (LLPS) has emerged as an important regulatory mechanism in cancer biology and has been implicated in hepatocellular carcinoma (HCC) progression. LLPS has also been linked to ferroptosis, a regulated cell death process with tumor-suppressive potential. However, how LLPS-related regulators modulate ferroptosis in HCC remain unclear. Here, we report the precise mechanism of TRIM21 in regulating the susceptibility of HCC to ferroptosis. <i>Methods</i> Bioinformatics analysis was employed to evaluate TRIM21 expression in HCC and identify ferroptosis suppressors potentially associated with TRIM21. In vitro experiments were then conducted to assess the impact of TRIM21 on cell malignant phenotypes. Finally, immunofluorescence and FRAP experiments were carried out to investigate the phase separation phenomenon of TRIM21. <i>Results</i> TRIM21 was found to be upregulated in HCC and associated with prognosis. Bioinformatic screening identified EZH2 as a candidate ferroptosis suppressor associated with TRIM21. TRIM21 knockdown enhanced ferroptosis sensitivity in HCC cells and suppressed malignant phenotypes. Mechanistically, TRIM21 underwent LLPS that depended on its coiled-coil domain (a predicted IDR region). Co-immunoprecipitation assays and immunofluorescence further supported a molecular association between TRIM21 and EZH2. Disruption of LLPS by TRIM21 mutant effectively abolished its cytoplasmic colocalization with EZH2, thereby attenuating the invasive capacity of HCC cells. <i>Conclusion</i> This study demonstrates that TRIM21 inhibits ferroptosis through LLPS, thereby promoting HCC cell survival. These findings reveal a previously unrecognized link between TRIM21 LLPS, ferroptosis, and HCC progression, providing a rational basis for targeting LLPS mechanisms to treat HCC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00968-y.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"100"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812087","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":"TM4SF1 regulates esophageal squamous cell carcinoma KYSE150 cell phenotypes via miRNA-regulated pathways.","authors":"Annatasha Stephen, Yuan Seng Wu, Nur Syafiqah Rahim, Bernadette Xin Jie Tune, Michelle Felicia Lee, Abbas Khan, Maw Shin Sim, Najihah Mohd Hashim, Appalaraju Velaga","doi":"10.1007/s10616-026-00962-4","DOIUrl":"https://doi.org/10.1007/s10616-026-00962-4","url":null,"abstract":"<p><p>TM4SF1, a small transmembrane glycoprotein, has been implicated in tumor progression across multiple cancers. However, its functional and regulatory roles in esophageal cancer, particularly esophageal squamous cell carcinoma (ESCC), remain unclear. This study aims to characterize TM4SF1 expression in an ESCC cell line, KYSE150, determine its biological role in tumor cell phenotypes, and profile miRNA changes after <i>TM4SF1</i> knockdown and perform in silico target or pathway analyses. First, <i>TM4SF1</i> gene expression was analyzed in the KYSE150 cell line by qRT-PCR. shRNA-mediated <i>TM4SF1</i> knockdown was applied to the KYSE150 cells, followed by proliferation, migration, and apoptosis assays. MiRNA sequencing followed by bioinformatic analyses predicted microRNAs and potential genes targeting TM4SF1, which also included putative composite pathways and gene ontologies. <i>TM4SF1</i> gene expression was significantly upregulated in the KYSE150 cells compared to EC109 ESCC and HET1A cells, a normal esophageal epithelial cell. Functional bioassays revealed that <i>TM4SF1</i> knockdown significantly reduced cell proliferation (MTT and CCK-8 assays) by 46%, while reducing wound closure at 24 h by 30.5% with recovery by 48 h and increased 90% of caspase 3/7 activity. The exploratory sequencing of miRNAs revealed the ten most differentially expressed miRNAs (hsa-miR-6510-3p, hsa-miR-675-5p, hsa-miR-524-5p, hsa-miR-9902, hsa-miR-520f-3p, hsa-miR-3192-5p, hsa-miR-1973, hsa-miR-3614-5p, hsa-miR-501-3p, and hsa-miR-1298-5p), whereas bioinformatic analyses predicted 54 target gene predictions, including TP53, RB1, and ICAM3, and 13 composite pathways that encompassed processes such as apoptosis, cell adhesion, and metabolic regulation. This study provides preliminary and useful insights into the role of TM4SF1 within the KYSE150 ESCC cell-line model and provide a basis for future validation in additional ESCC models, alongside initial investigations into its molecular mechanisms, and underscores the necessity of further validation in diverse cells and models and possible therapeutic implications.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"95"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13103068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765070","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 perioperative anesthesia-associated signature in Kawasaki disease patients with deep vein thrombosis; evidence from machine-learning driven multi-omics.","authors":"Ling Niu, Fengmei Tang, Min Ren","doi":"10.1007/s10616-026-00946-4","DOIUrl":"https://doi.org/10.1007/s10616-026-00946-4","url":null,"abstract":"<p><p>Inappropriate perioperative anesthesia (PA) drug management may lead to the detrimental clinical outcomes of Kawasaki disease (KD) patients with deep vein thrombosis (DVT). However, perioperative anesthesia-related drug target genes(PADTGs) role in KD patients with DVT has not yet been elucidated. This study aims to decipher PARDTGs molecular patterns in KD patients with DVT via machine learning-assisted multi-omics. By integrating 3 DVT bulk datasets (GSE118259, GSE19151, GSE48000) and 3 machine learning pipelines(RF, Lasso and SVM-RFE), we discovered the PARDTGs-associated DEGs and hub genes for DVT patients. Consensus clustering and nomogram were utilized for identifying PARTGs-associated molecular subgroups for DVT patients in GSE19151 and dignostic model for DVT and KD patients in aforementioned 3 DVT bulk datasets and 2 KD bulk profiles(GSE68004 and GSE18606). Indeed, hub gene molecular and immune features were estimated in DVT bulk profiles(GSE19151) and KD single-cell data(GSE254657) at temporal and spatial manners. Besides, Therapeutic agent targeting hub gene in purpose of reversing DVT and KD to healthy status were enriched by CTD database, and validated by molecular docking. In addition, an in vitro KD model further validated hub gene expression. PTMA and FTHL8 were identified as 2 PARDTGs-associated signatures involved in KD patients for forecasting DVT pathogenesis, which was mainly distributed in neutrophils of KD patient peripheral blood. Besides, Gallic acid can be considered as reproposing approaches for treatment DVT in KD patients. Our study systemically discovered PARDTGs-related signature involved in DVT pathogenesis of KD patients via machine learning-driven multi-omics, which provides novel idea in their clinical application.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00946-4.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"93"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721796","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":"Naringenin suppresses colorectal Cancer progression by targeting the Gankyrin/PI3K /AKT/GSK-3β/β-catenin signaling Axis.","authors":"Chengxing Wang, Weixing Lin, Chunbo Wu, Chaorong Zhou, Yuan Gao, Yongfeng Ma, Canxiu He, Jianchang Wei, Lianmei Li, Rihui Wu, Jinglin Zhao, Yaoming He","doi":"10.1007/s10616-026-00948-2","DOIUrl":"https://doi.org/10.1007/s10616-026-00948-2","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains one of the most prevalent and lethal malignancies worldwide. Natural products derived from Traditional Chinese Medicine (TCM), offer promising therapeutic potential due to their multitarget effects and low toxicity. Naringenin (NAR), a major flavonoid found in citrus peel (chenpi), has shown anticancer activity in several tumor types; however, its mechanism in CRC remains incompletely understood. We combined network pharmacology, molecular docking, and experimental validation to explore the anti-CRC mechanisms of NAR. Bioinformatics databases were used to identify overlapping targets between NAR and CRC. Enrichment analyses and protein-protein interaction (PPI) networks were performed. The interaction between NAR and core targets was confirmed <i>via</i> molecular docking. In vitro assays (CCK-8, colony formation, flow cytometry, Transwell) and Western blotting were used to assess the functional and molecular effects of NAR and Gankyrin modulation. In vivo efficacy and toxicity were evaluated using a CRC xenograft model in nude mice. Network pharmacology identified AKT1 as a hub target, and pathway enrichment highlighted PI3K-AKT signalling. Naringenin (NAR) dose-dependently suppressed colorectal cancer (CRC) cell proliferation, migration and invasion, while promoting apoptosis. In vivo, NAR significantly inhibited tumour growth without overt systemic toxicity. Mechanistically, NAR attenuated the Gankyrin-PI3K-AKT-GSK-3β-β-catenin axis. In gain-of-function rescue experiments, Gankyrin overexpression partially blunted the anti-proliferative and anti-invasive effects of NAR, supporting a Gankyrin-dependent component of NAR activity. This study reveals that NAR exerts anti-CRC effects by targeting the Gankyrin/ PI3K/AKT/GSK-3β/β-catenin pathway, supporting its potential as a safe and effective therapeutic agent in CRC treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00948-2.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 3","pages":"86"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671058","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}