Cytotechnology最新文献

{"title":"A simplified in vitro disease-mimicking culture system can determine the angiogenic effect of medicines on vascular diseases.","authors":"SongHo Moon, Yuzuru Ito","doi":"10.1007/s10616-025-00736-4","DOIUrl":"10.1007/s10616-025-00736-4","url":null,"abstract":"<p><p>Many patients undergoing clinical regenerative treatments experience severe conditions arising from endothelial disruption. In chronic cardiac and perivascular diseases, deficiencies in vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), and heparin, which are essential for maintaining and activating endothelial cells, can lead to angiogenic dysregulation. Endothelial disruption caused by ischemic hypoxia and a deficiency in these factors is associated with many vascular diseases. However, their pathogenic processes remain unclear at the cellular level. Therefore, the present study aimed to develop a culture system that mimics the disease environment to test the effectiveness of drug candidates in restoring damaged blood vessels in chronic vascular diseases, including coronary artery disease and peripheral vascular disease. This study focused on VEGF, IGF, and heparin and developed a pseudo-disease culture system by pre-treating human umbilical vein endothelial cells (HUVECs) with a starvation medium (EGM-2™ medium lacking VEGF, IGF, and heparin) to examine the ability of HUVECs to form a traditional 2D vascular network. The results indicated that a deficiency in these proteins results in disruptions in tube morphogenesis. Moreover, the results suggested that dysregulation of the PI3K/AKT pathway plays a key role for in vascular disruption in HUVECs. The proposed pseudo-disease starvation system provides a simple way to visualize pathological disruptions to blood vessels and assess the efficacy of drugs for vascular regeneration.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00736-4.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"75"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585006","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":"Mechanism underlying the role of the circRNA OMA1/miR-654-3p/RAF1 axis in children with inflammatory bowel disease.","authors":"Ping Zhang, Zhenhui Wang, Yufen Xu, Meirong Wu","doi":"10.1007/s10616-025-00703-z","DOIUrl":"10.1007/s10616-025-00703-z","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), a chronic gastrointestinal disorder, often emerges during childhood and poses significant challenges due to its adverse effects on growth, development, and psychosocial well-being. Circular RNAs (circRNAs) have been implicated in the pathogenesis of diverse diseases. However, the specific biological role and mechanisms of circRNA OMA1 in children with IBD remain largely unexplored. This study investigates the functions and mechanistic pathways of circRNA OMA1 in the progression of IBD. Quantitative real-time PCR (qRT-PCR) was employed to quantify circRNA OMA1 and miR-654-3p expression levels in the serum of children with IBD and in HT-29 cells. Downstream miRNA and mRNA targets of circRNA OMA1 were predicted using StarBase and validated via luciferase reporter assays. An in vitro IBD model was established by treating the human colonic epithelial cell line (HT-29) with 2% dextran sulfate sodium (DSS). Cell viability and apoptosis were assessed using the MTT assay and flow cytometry, respectively. Expression of the apoptosis-related protein cleaved caspase-3 was analyzed via western blotting, and proinflammatory cytokine levels (TNF-α, IL-1β, and IL-6) were measured using ELISA. The expression of circRNA OMA1 was notably lower in the serum of children with IBD and in DSS-treated HT-29 cells than in healthy controls, whereas miR-654-3p expression was upregulated. Bioinformatics analyses revealed a direct interaction between circRNA OMA1 and miR-654-3p. Overexpression of circRNA OMA1 through plasmid transfection increased circRNA OMA1 levels and suppressed miR-654-3p expression in HT-29 cells under both basal and DSS-stimulated conditions. Conversely, transfection with a miR-654-3p mimic reversed these effects. Upregulation of circRNA OMA1 ameliorated DSS-induced injury in HT-29 cells by enhancing cell viability, reducing apoptosis, and downregulating cleaved caspase-3 expression. Moreover, circRNA OMA1 overexpression inhibited the secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6. However, these protective effects were partially reversed by treatment with the miR-654-3p mimic. Additionally, miR-654-3p was shown to directly target RAF1, negatively regulating its expression. The proliferation-promoting and apoptosis-suppressing effects of miR-654-3p inhibitor treatment were mitigated by RAF1-siRNA. <i>Conclusion:</i> Upregulation of circRNA OMA1 alleviates DSS-induced colonic cell apoptosis and inflammation by modulating the miR-654-3p/RAF1 axis. These findings suggest that circRNA OMA1 could be a promising biomarker for the diagnosis and treatment of IBD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00703-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"42"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045787","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":"Expression profiling of circular RNAs in sepsis-induced acute gastrointestinal injury: insights into potential biomarkers and mechanisms.","authors":"Xiaojun Liu, Chenxi Li, Chengying Hong, Yuting Chen, Chuanchuan Nan, Silin Liang, Huaisheng Chen","doi":"10.1007/s10616-025-00704-y","DOIUrl":"10.1007/s10616-025-00704-y","url":null,"abstract":"<p><p>This study aimed to investigate the role of circular RNAs (circRNAs) in sepsis-induced acute gastrointestinal injury (AGI), focusing on their potential as biomarkers and their involvement in disease progression. Peripheral blood samples from 14 patients with sepsis-induced AGI and healthy volunteers were collected. RNA sequencing was performed to profile circRNA and miRNA expression. Differential expression analysis identified key regulatory RNAs. Functional enrichment analysis was conducted to explore biological pathways, and circRNA-miRNA interaction networks were constructed. Significant differences in circRNA and miRNA expression profiles were observed between sepsis-induced AGI patients and healthy controls. Several circRNAs, including hsa_circ_0008381 and hsa_circ_0071375, exhibited stepwise expression increases correlating with AGI severity. Functional enrichment analysis indicated that the host genes of differentially expressed circRNAs are involved in key biological processes like protein ubiquitination, organelle maintenance, and cellular signaling pathways such as mitochondrial biogenesis and lipid metabolism. CircRNA-miRNA interaction networks suggested their role as miRNA sponges, regulating key downstream processes. This study demonstrated the potential of circRNAs as diagnostic biomarkers and therapeutic targets for sepsis-induced AGI. Further research is warranted to validate their clinical utility and unravel their mechanistic roles in AGI progression.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"43"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045424","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":"Esketamine alleviated cardiomyocyte ferroptosis induced by oxygen-glucose deprivation/reoxygenation (OGD/R) via cyclic GMP-AMP synthase interactor.","authors":"Jianjun Ouyang, Weiqiang Xiao, Di Wu, Manyun Bai, Qian Zhao, Yufang Li","doi":"10.1007/s10616-025-00723-9","DOIUrl":"10.1007/s10616-025-00723-9","url":null,"abstract":"<p><strong>Background: </strong>The use of tourniquets (TQ) during the total knee arthroplasty (TKA) induced ischemia-reperfusion (I/R) injury in the limb, resulting in the release of inflammatory cytokines and reactive oxygen species (ROS), therefore leading to myocardial damage. This study aimed to investigate the effects and molecular mechanism of Esketamine on myocardial injury (MI) caused by TQ-induced I/R injury.</p><p><strong>Methods: </strong>A randomized numerical table method was used to divide 23 patients into the C group (11 cases, ACB + conventional anesthesia) and M group (12 cases, ACB + conventional anesthesia + 0.5 mg/kg Esketamine). The levels of lactate dehydrogenase (LDH), Malondialdehyde (MDA), Fe²⁺, Glutathione Peroxidase (GSH-Px), glutathione (GSH), IL-6, TNF-α, Creatine Kinase (CK) and CreatineKinase-MB (CKMB) were determined by reagent kits. The expression of CGAMP interaction factor (STING), Glutathione Peroxidase 4 (GPX4), and Ferritin Heavy Chain 1 (FTH1) was examined by Western blot. The ROS level was tested by flow cytometry. The expression of STING was validated by immunofluorescence.</p><p><strong>Results: </strong>Compared with the C group, the levels of GSH-Px and GSH were increased while the levels of IL-6, TNF-α, MDA, Fe²⁺, CK, CKMB, and LDH were decreased in the M group. Furthermore, esketamine relieved the OGD/R-induced increase of MDA, Fe²⁺, and ROS and the decrease of GSH-Px, GSH, GPX4, and FTH1, which were reversed by STING overexpression.</p><p><strong>Conclusion: </strong>Esketamine alleviated cardiomyocyte ferroptosis via STING, which might be the molecular mechanism of Esketamine to ameliorate the MI caused by TQ-induced I/R injury.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00723-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"57"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11807036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390450","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":"DNA methyltransferase DNMT3A inhibits TP53AIP1 expression and promotes cervical cancer development and metastasis.","authors":"Xiaohong Pan, Xiuluan Du, Suhong Jia","doi":"10.1007/s10616-025-00735-5","DOIUrl":"10.1007/s10616-025-00735-5","url":null,"abstract":"<p><p>Cervical cancer (CC) patients have a poor prognosis and a low 1-year survival rate due to recurrence or pelvic metastasis. The GSE9750 dataset was analyzed to identify hub genes in CC. CCK-8, colony formation assay, EdU, TUNEL, Transwell assays, and western blot analysis for apoptosis-associated markers were conducted to examine CC cell malignant phenotype after different lentiviral vector treatments. Dual-luciferase assay, ChIP, and MSP were used for regulatory assays. P53-regulated apoptosis-inducing protein 1 (TP53AIP1) was lowly expressed in CC tissues and cell lines, and TP53AIP1 overexpression repressed proliferation, migration, and invasion, and induced apoptosis of CC cells by activating the p53 signaling. DNMT3A bound to the TP53AIP1 promoter and transcriptionally repressed TP53AIP1 expression. DNA-methyltransferase 3A (DNMT3A) silencing inhibited CC development and lung metastasis in vivo, but further TP53AIP1 knockdown reversed this phenomenon by disrupting p53-mediated apoptosis. In summary, DNMT3A transcriptionally repressed TP53AIP1 expression to promote CC progression and metastasis.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"74"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585007","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":"AKT activation participates in Fascin-1-induced EMT in hepatoma cells.","authors":"Pengju Zhao, Kewei Ai, Yi Li, Wei Cheng, Jiwu Yang","doi":"10.1007/s10616-025-00707-9","DOIUrl":"10.1007/s10616-025-00707-9","url":null,"abstract":"<p><p>High expression of Fascin-1 involves high metastasis, high recurrence, and poor prognosis of cancers. However, the related regulatory mechanism in hepatocellular carcinoma (HCC) remains elusive. In this study, Fascin-1 was highly expressed in HCC tissues and cell lines. Fastin-1 protein levels and p-Akt1/Akt1 rate were increased by Akt activator SC79 and were decreased by Akt inhibitor LY294002. Silenced Fascin-1 suppressed cell proliferation, promoted cell apoptosis, suppressed cell invasion and epithelial-mesenchymal transition (EMT) in HCC cell lines. Also, silenced Fascin-1 induced cell cycle arrest in the G1 phase. Moreover, silenced Fascin-1 repressed invasion of HCC cells by inhibiting EMT. Besides, interference with Fascin-1 inhibited HCC cell growth, reduced Vimentin expressions and p-Akt1/Akt1 rate in vivo, while these impacts were abolished after injection of SC79. In conclusion, silencing Fascin-1 reduced the malignant growth of HCC, and this process was closely related to AKT inactivation.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00707-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"46"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045310","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":"BSP promotes skin wound healing by regulating the expression level of SCEL.","authors":"Yan Wu, Chun-Yu Li","doi":"10.1007/s10616-025-00712-y","DOIUrl":"10.1007/s10616-025-00712-y","url":null,"abstract":"<p><p>Burn injuries are complex, life-threatening events involving intricate cellular and molecular processes, including angiogenesis, which is vital for effective wound healing. <i>Bletilla striata</i> polysaccharide (BSP), a bioactive compound from <i>Bletilla striata</i>, exhibits anti-inflammatory and wound-healing properties. However, its impact on angiogenesis modulation, particularly through the synaptopodin-2-like (SCEL) gene, remains poorly understood. The effects of BSP on HMEC-1 cells exposed to lipopolysaccharide (LPS) were assessed using cell viability, migration, apoptosis, and angiogenesis assays. SCEL's role was explored through lentiviral transfection to manipulate SCEL expression. Animal models were employed to evaluate BSP's therapeutic potential in burn wound healing, with histological analysis, immunohistochemistry (IHC), and molecular assays to assess tissue repair and angiogenesis. BSP significantly alleviated LPS-induced damage in HMEC-1 cells by promoting cell survival, reducing apoptosis, and enhancing migration and angiogenesis. BSP treatment downregulated SCEL expression, reversing LPS-induced cellular damage. In SCEL-overexpressing cells and mice, BSP's beneficial effects on wound healing were attenuated, indicating SCEL's regulatory role in angiogenesis. In vivo, BSP accelerated burn wound closure, improved tissue organization, and enhanced angiogenesis, as evidenced by increased CD31 expression. SCEL overexpression impaired these effects, highlighting the essential role of SCEL downregulation in BSP-mediated healing. BSP promotes burn wound healing by modulating angiogenesis via SCEL downregulation, facilitating cell survival, migration, and vascularization. These findings position BSP as a promising therapeutic agent for burn wound treatment, with further investigation into SCEL's molecular mechanisms offering potential for novel wound care strategies.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"49"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045437","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":"E2F2 induces microglial activation and augments depressive-like behavior in mice by repressing PTPN6 transcription.","authors":"Jiali Xin, Yao Chen, Leijing Zhang, Lan Ma","doi":"10.1007/s10616-025-00730-w","DOIUrl":"10.1007/s10616-025-00730-w","url":null,"abstract":"<p><p>Depression is the leading contributor to disability and suicide ideation. Informed by the insights from bioinformatics analyses, this study investigates the roles of E2F transcription factor 2 (E2F2) and protein tyrosine phosphatase non-receptor type 6 (PTPN6) in the activation of microglia and the manifestation of depressive-like behavior in mice. Chronic unpredictable mild stress was applied <b>t</b>o induce a mouse model of depression, while a cellular model featuring microglia was established through exposure to lipopolysaccharide and adenosine triphosphate. E2F2 was upregulated whereas PTPN6 was downregulated in these models. Notably, E2F2 was found to bind to the PTPN6 promoter, thereby repressing its transcription. Various behavioral tests demonstrated that silencing of E2F2, accomplished via shRNA transfection, led to increased locomotor activity, heightened social interaction rates, enhanced sucrose preference, and reduced immobility time in response to stress stimuli in mice. Furthermore, E2F2 silencing effectively reduced expression of Iba1, a microglial activation marker, and decreased concentrations of pro-inflammatory cytokines both in vivo and in vitro. However, these mitigating effects were countered by additional PTPN6 silencing. In conclusion, this study investigation underscores the role of E2F2 in promoting inflammatory activation of microglia and exacerbating depressive-like behavior in mice by repressing PTPN6 transcription.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"66"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11845659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482472","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":"Cell culture in salivary gland tumor research: molecular insights of pathogenic targets and personalized medicine.","authors":"Mayara Trevizol Gonçalves, Luccas Lavareze, Erika Said Abu Egal, Albina Altemani, Fernanda Viviane Mariano","doi":"10.1007/s10616-025-00726-6","DOIUrl":"10.1007/s10616-025-00726-6","url":null,"abstract":"<p><p>Salivary gland tumors (SGT) are a diverse group of tumors with various subtypes and morphological characteristics. Cell culture is a low-cost technique used as a valuable tool for studying cancer behavior and molecular characteristics. In vitro studies may offer a controlled environment for initial investigations before conducting in vivo experiments, making them indispensable in cancer research, drug testing, and personalized medicine. SGT cell culture techniques have been utilized to establish cell lines that provide insight into the genetic and molecular alterations underlying these tumors, aiding in the identification of potential therapeutic targets. Here, we highlight the application of cell culture techniques in studying SGT, emphasizing their contribution to advancements in understanding tumor behavior and potential novel therapeutic strategies.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"70"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540495","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":"FXYD6 is transcriptionally activated by KLF10 to suppress the aggressiveness of gastric cancer cells.","authors":"Chao Liu, Xin Zhou, Guangsheng Wang, Chenyu Zhu, Rui Xu","doi":"10.1007/s10616-025-00710-0","DOIUrl":"10.1007/s10616-025-00710-0","url":null,"abstract":"<p><p>Despite improvements in therapeutic approaches, the mortality rate of gastric cancer (GC) remains unacceptably high. Evidence suggests that FXYD domain containing ion transport regulator 6 (FXYD6) is downregulated in GC. However, its exact function and the molecular mechanism in GC are still unclear. FXYD6 expression in different cell lines was estimated using RT-qPCR. Western blotting was employed for protein expression detection. Cell counting kit-8 assay, colony formation assay, and flow cytometry were implemented to assess GC cell viability, proliferation, and apoptosis, respectively. Bioinformatics analysis as well as chromatin immunoprecipitation and luciferase reporter assays were utilized for verifying FXYD6 interaction with the transcription factor Krüppel-like factor 10 (KLF10). The results showed that FXYD6 displayed a decreased level in GC cell lines. Impaired proliferative ability and enhanced apoptotic capacity were observed in GC cells overexpressing FXYD6. KLF10 expression is positively correlated with FXYD6 expression in GC samples. KLF10 binds to the FXYD6 promoter to enhance its transcription. FXYD6 depletion counteracted KLF10 upregulation-triggered reduction in GC cell proliferation and elevation in apoptosis. In conclusion, KLF10 activates FXYD6 transcription, thereby impeding GC cell proliferation and promoting cell apoptosis.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"48"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045427","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}