Cytotechnology最新文献

{"title":"Yunnan medicine Jiangzhi ointment alleviates hyperlipid-induced hepatocyte ferroptosis by activating AMPK and promoting autophagy.","authors":"Xin Hong, Haijing Liu, Hongli Sun, Yan Zhuang, Meizhen Xiao, Shaoping Li, Yandong Li, Ming Jing","doi":"10.1007/s10616-025-00737-3","DOIUrl":"10.1007/s10616-025-00737-3","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) is a serious public health problem worldwide. The purpose of this study was to investigate whether Yunnan medicine Jiangzhi ointment (YMJO) can relieve the progression of NAFLD and to elucidate the specific mechanism involved. A NAFLD model was established in high-fat diet (HFD)-induced SD rats and free fatty acid (FFA)-induced BRL 3A cells. The expression of autophagy-related proteins and ferroptosis-related proteins was detected using Western blotting. The histopathological features of the livers of NAFLD rats were evaluated using hematoxylin and eosin (HE) and Oil Red O staining. The results revealed that in a successfully established HFD-induced NAFLD rat model, YMJO alleviated the progression of NAFLD, promoted autophagy, and inhibited ferroptosis. This regulatory mechanism is related to the activation of the AMPK pathway. Further study of the molecular mechanism via cell experiments revealed that YMJO activated FFA-induced liver cell autophagy through the AMPK signaling pathway and inhibited ferroptosis, thus alleviating the development of NAFLD. This study revealed that YMJO promotes phosphorylation by activating the AMPK pathway, enhances autophagy, ameliorates ferroptosis induced by high fat, and alleviates the occurrence and development of NAFLD.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"73"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585008","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":"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":"circDHX33 suppresses glycolysis, malignant proliferation, and metastasis in prostate cancer by interacting with RNA-binding protein IGF2BP2 to destabilize its protein.","authors":"XiangDong Liang, XiaoLiang Tan, Long Pei, ChunHui Dong","doi":"10.1007/s10616-025-00718-6","DOIUrl":"10.1007/s10616-025-00718-6","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a malignant tumor characterized by dependence on androgens and enhanced glycolytic processes in response to the energy demands of rapid proliferation. This study delved into the role of circDHX33 interacting with IGF2BP2 in regulating the malignant behavior of PCa. circRNA expression data from PCa tissues and normal tissues were selected from the GEO database, and differentially expressed circRNAs were screened out. circDHX33 expression in clinical PCa samples was verified by RT-qPCR. Cellular experiments included cell culture, RNA interference and overexpression assays, as well as the use of Transwell migration invasion assay and EdU cell proliferation assay to assess the effect of circDHX33 on the proliferation and migration of PC-3 cells. In addition, its regulatory effect on energy metabolism in tumor cells was assessed by glycolysis assay. FISH assay, RNA pull-down, silver staining assay, and RIP were used to evaluate the interaction between circDHX33 and IGF2BP2. circDHX33 expression was significantly reduced in PCa tissues relative to normal tissues. Overexpression of circDHX33 significantly inhibited the glycolytic activity, proliferative capacity, and migratory and invasive abilities of PC-3 cells, and this effect was closely related to its reduction of IGF2BP2 protein stability. Knockdown of IGF2BP2 could reverse the malignant behavior of cells enhanced by circDHX33 knockdown. In addition, the direct intracellular interaction between circDHX33 and IGF2BP2 was verified. circDHX33 inhibits glycolysis and malignant proliferation in PCa through interaction with IGF2BP2, suggesting its potential as a potential therapeutic target.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"56"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11802939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381845","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":"Autotaxin regulates the expression and the activity of P-glycoprotein in lipopolysaccharide -activated microglial cells.","authors":"Mohammad Fayyad-Kazan, Zeina Soayfane, Wissam Faour, Hussein Fayyad-Kazan, Rana Awada","doi":"10.1007/s10616-025-00727-5","DOIUrl":"10.1007/s10616-025-00727-5","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs), such as Alzheimer's and Parkinson's, are characterized by chronic inflammation and oxidative stress, often mediated by activated microglial cells. Microglia-induced neuroinflammation is essential to neuronal damage, driven by the overproduction of pro-inflammatory cytokines and reactive oxygen species. Autotaxin (ATX), a lysophospholipase D enzyme, can modulate inflammation through its enzymatic product lysophosphatidic acid (LPA). While previous studies highlighted ATX's anti-inflammatory properties, its impact on P-glycoprotein (P-gp), a key efflux transporter involved in drug resistance and neuroinflammation, remains not fully understood. The objective of this study was to explore how ATX modulates the expression and activity of P-gp in lipopolysaccharide (LPS)-activated and H2O2-stressed BV-2 microglial cells. Microglial cells were transfected with either an empty vector (EV) or an ATX cDNA vector (A +) and exposed to LPS (1 µg/mL) or H2O2 (100 µM). The mRNA expression levels of P-gp and pro-inflammatory cytokines were analyzed using qRT-PCR, and P-gp activity was assessed using the NBD-CSA fluorescence efflux assay. Our findings revealed that while LPS- and H₂O₂-treated microglial cells were characterized by an abnormal cellular morphology with long ramified processes, ATX overexpression restored the round shape morphology normally observed in the control untreated cells. Interestingly, ATX overexpression significantly reduced the mRNA levels of pro-inflammatory cytokines, such as TNF-<i>α</i>, in LPS- and H₂O₂-treated microglial cells. Moreover, ATX overexpression reduced both the mRNA levels and efflux activity of P-gp under inflammatory and oxidative stress conditions. These results suggest that ATX mitigates microglial activation and its downstream effects, highlighting its therapeutic potential in reducing neuroinflammation.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"58"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11822174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432667","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 mechanism of curcumin protecting against IL-1β-induced oxidative stress and inflammation in chondrocytes via the Bmp2/Smad5/Runx2 pathway.","authors":"Jinlei Li, Weitong Liu, Tao Wang, Yanbo Wang, Guang Yang, Jiankun Chen, Yongsheng Xu, Jingfan Yang","doi":"10.1007/s10616-025-00731-9","DOIUrl":"10.1007/s10616-025-00731-9","url":null,"abstract":"<p><p>A core role of chondrocyte survival/death has been suggested in the pathogenesis of osteoarthritis. We explored the underlying molecular mechanism of curcumin protecting against interleukin-1β (IL-1β)-induced chondrocyte injury via the bone morphogenetic protein 2 (Bmp2)/small mothers against decapentaplegic homolog 5 (Smad5)/runt-related transcription factor 2 (Runx2) pathway. Chondrocytes ATDC5 in vitro inflammatory model was established by IL-1β induction, and treated with curcumin, or Smad5 small interfering RNA. Levels of extracellular matrix (ECM) type II collagen (Col-II) and aggrecan, reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and IL-6 were determined by immunocytochemistry, kits and ELISA. Apoptosis and necrosis were assessed by Annexin V/PI and TUNEL. Matrix metalloproteinase 13 (MMP13), A disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5), Bmp2/Smad5/Runx2 expression and Smad5 phosphorylation levels were determined by qPCR and western blot. IL-1β-treated ATDC5 cells showed decreased Col-II, aggrecan in ECM and SOD and GSH-Px levels, as well as increased apoptosis and levels of MMP13, ADAMTS5, Bmp2, Runx2, ROS, COX-2, TNF-α and IL-6 and Smad5 phosphorylation (all <i>p</i> < 0.05), whilst curcumin treatment brought about the opposite trends, suggesting that curcumin inhibited oxidative stress, inflammatory response and apoptosis, and inactivated the Bmp2/Smad5/Runx2 pathway in IL-1β-treated chondrocytes. Additionally, Smad5 silencing also caused suppressed oxidative stress, inflammatory response and apoptosis in IL-1β-treated chondrocytes. Curcumin reduced IL-1β-induced chondrocyte oxidative stress, inflammation, and apoptosis, and increased ECM secretion by inactivating the Bmp2/Smad5/Runx2 pathway, thereby exerting a protective effect on injured chondrocytes.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"71"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11871223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540496","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":"β-sitosterol in Yijing Hugui decoction prevents cyclophosphamide-induced premature ovarian insufficiency via the AKT1/Nrf2 pathway.","authors":"Li Chen, Li Zeng, Shuyu Pan, Li Zu, Hongyan Pan, Li Fan","doi":"10.1007/s10616-025-00740-8","DOIUrl":"10.1007/s10616-025-00740-8","url":null,"abstract":"<p><p>Premature ovarian insufficiency (POI) is a condition marked by premature depletion of ovarian function, affecting a significant portion of women. The objective of this study is to assess the therapeutic efficacy of Yijing Hugui decoction (YJHGD) in the treatment of POI and to elucidate its pharmacological mechanisms. In this study, network pharmacology was used to identify key bioactive compounds in YJHGD, and the components were characterized using LC-MS. In vitro, we used KGN cells treated with cyclophosphamide (CP) to model POI. In vivo, a CP-induced POI mouse model was established. The in vitro therapeutic effects of β-sitosterol on CP-treated KGN cells were evaluated through various parameters. These parameters encompass cell viability, oxidative markers, antioxidant indexes, ATP concentration, intracellular ROS levels, apoptosis rate, and apoptosis-related protein expression. The in vivo therapeutic effects of β-sitosterol in POI mice were assessed through H&E staining, circulating reproductive hormone level detection, reproductive hormone receptor expression measurement, oxidative stress profile, and apoptosis assay. The potential protein target of β-sitosterol was identified utilizing molecular docking in conjunction with drug affinity responsive target stability (DARTS). β-sitosterol was identified as a major active component of YJHGD contributing to its therapeutic effects. In β-sitosterol-treated KGN human granulosa cells, oxidative stress and apoptosis were significantly reduced (<i>P</i> < 0.05). The interaction between β-sitosterol and AKT1 was verified. Furthermore, β-sitosterol significantly activated the AKT1/Nrf2 signaling pathway in vivo and in vitro (<i>P</i> < 0.05). AKT1 activator insulin significantly alleviated CP-induced oxidative stress (<i>P</i> < 0.05). Our results suggest that β-sitosterol inhibits oxidative stress and apoptosis by targeting AKT1 and activating the Keap1/Nrf2/HO-1 signaling. In vivo studies demonstrated that β-sitosterol significantly restored ovarian tissue damage in mice, reduced the circulating levels of reproductive hormones, downregulated the expression of reproductive hormone receptors, alleviated oxidative stress and ROS generation, and improved apoptosis (<i>P</i> < 0.05), which was achieved through the AKT1/Nrf2 pathway. In Conclusion, YJHGD possesses therapeutic potential for the treatment of POI. The active compound, β-sitosterol, demonstrated significant anti-POI effects through its interaction with AKT1, leading to the activation of AKT1/Nrf2 signaling pathway. This interaction contributes to the reduction of oxidative stress and the prevention of cellular apoptosis. Our results suggest that β-sitosterol may represent a novel therapeutic approach.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00740-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"76"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613859","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":"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}