Cytotechnology最新文献

{"title":"Correction: Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes.","authors":"Jaldeep Langhnoja, Lipi Buch, Prakash Pillai","doi":"10.1007/s10616-025-00743-5","DOIUrl":"https://doi.org/10.1007/s10616-025-00743-5","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-024-00698-z.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"85"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794809","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":"Functional changes in β-lactoglobulin by conjugation with carboxymethyl cellulose.","authors":"Tatsuya Arai, Moeko Ono, Maiko Yoneda, Marika Sugamura, Tadashi Yoshida, Makoto Hattori","doi":"10.1007/s10616-025-00741-7","DOIUrl":"10.1007/s10616-025-00741-7","url":null,"abstract":"<p><p>β-lactoglobulin (BLG) and carboxymethylcellulose (CMC) were conjugated by using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC). The BLG-CMC conjugates with different CMC content and molecular weights were prepared. Confirmation of conjugation was carried out by SDS-PAGE. CD spectra revealed that the secondary structure of BLG had maintained in the conjugates. Fluorescence studies indicated that the conformation around Trp had not changed in the conjugates. Retinol-binding activity indicated that the retinol-binding site of BLG changed by the conjugation. Equilibrium constants (K_AS) of anti-BLG monoclonal antibodies (mAbs) to BLG after conjugating with CMC by competitive ELISA indicated that the structure around ¹⁵Val-²⁹Ile and ⁸Lys-¹⁹Trp maintained their native structure, and the structure around ¹²⁵Thr-¹³⁵Lys changed by conjugation. By conjugation with CMC, emulsifying property of BLG in the acidic pH region and in the presence of NaCl were much improved. Because acidic pH and salt are frequently used in food, the BLG-CMC conjugates are considered to be useful for food applications. Immunogenicity of BLG in BALB/c mice was reduced by this conjugation. In particular, there was a marked improvement in both emulsifying property and reduced immunogenicity in the BLG-high molecular weight (HMW) CMC conjugate. Therefore, conjugation with CMC is an effective way to improve BLG's function, and CMC with a high molecular weight is preferable.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"79"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRELP regulated by GAS5/miR-3127-5p suppresses cisplatin resistance in oral squamous cell carcinoma.","authors":"Xiaoni Sun, Yang Liu, Luyi Chai, Jianbo Zhou","doi":"10.1007/s10616-025-00749-z","DOIUrl":"https://doi.org/10.1007/s10616-025-00749-z","url":null,"abstract":"<p><p>Our previous study has identified that PRELP inhibits the progression of oral squamous cell carcinoma (OSCC). This study aimed to investigate the influence of PRELP on cisplatin (DDP) resistance in OSCC cells and to elucidate the underlying mechanism. The levels of PRELP, miR-3127-5p, and GAS5 in established DDP-resistant OSCC cell lines (CAL27/DDP and SCC-15/DDP) and parental cells were detected. Following transfection with PRELP overexpressing or silencing plasmids in DDP-resistant OSCC cells, DDP resistance was evaluated by the IC50 values, proliferation, apoptosis and ABCB1 expression. Bioinformatic analysis, dual-luciferase reporter assays, and rescue experiments were employed to explore the upstream miRNA and lncRNA of PRELP. Our results demonstrated that in both DDP-resistant cells, PRELP and GAS5 levels were decreased, while miR-3127-5p expression was increased compared with parental cells. PRELP overexpression reduced the IC50 of DDP and EdU-positive cell number, enhanced cell apoptosis, and suppressed ABCB1 expression in resistant cells. Conversely, PRELP silencing caused opposite effects. In the TCGA database, miR-3127-5p was highly expressed in HNSC, and patients with higher miR-3127-5p expression had shorter overall survival. A negative correlation was observed between miR-3127-5p and PRELP in HNSC. miR-3127-5p promoted DDP resistance in OSCC by targeting PRELP. GAS5 positively modulated PRELP expression by sponging miR-3127-5p. The alleviation of DDP resistance by GAS5 was attenuated by miR-3127-5p mimic and PRELP downregulation. In conclusion, PRELP, which is regulated by lncRNA GAS5/miR-3127-5p axis, suppresses DDP resistance in OSCC through decreasing ABCB1 expression. Targeting the GAS5/miR-3127-5p/PRELP axis may offer a promising strategy to overcome DDP resistance in OSCC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00749-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"92"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLGA microspheres loaded with si-circETS1 as a therapeutic strategy to delay intervertebral disc degeneration.","authors":"Wenlei Nie, Rong Zhang, Pingfeng Xie, Min Yang, Jiaming Wu","doi":"10.1007/s10616-025-00768-w","DOIUrl":"https://doi.org/10.1007/s10616-025-00768-w","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is one of the leading causes of chronic low back pain and functional impairment, severely affecting the quality of life of patients. In recent years, circular RNA (circRNA), has gained attention for its critical role in cellular function regulation, especially its potential therapeutic effects in IDD. This study aims to elucidate the function of circETS1 in nucleus pulposus cells (NPCs) and develop a novel targeted therapeutic strategy. CircETS1, which was abnormally highly expressed in degenerated nucleus pulposus tissue, was identified through circRNA sequencing (circRNA-seq). The circular nature of circETS1 was confirmed by Sanger sequencing, RNase R digestion, and fluorescence in situ hybridization (FISH). Primary human NPCs were cultured, and the effects of regulating circETS1 on cell proliferation, apoptosis, and extracellular matrix metabolism were studied using reverse transcription quantitative polymerase chain reaction (RT-qPCR), Western blotting, flow cytometry, and immunofluorescence. Polylactic-<i>co</i>-glycolic acid (PLGA) microspheres (MS) loaded with si-circETS1 were prepared, and their therapeutic effects were evaluated. PLGA MS loaded with si-circETS1 effectively delivered si-circETS1 to nucleus pulposus tissue in both in vitro and in vivo experiments, significantly downregulating circETS1 expression, reducing inflammation, promoting extracellular matrix synthesis and repair, and ultimately delaying the progression of IDD. Consequently, PLGA MS loaded with si-circETS1 present an innovative and promising therapeutic strategy for IDD, demonstrating strong potential for clinical application.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"99"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12075713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TUBB4A relieves high glucose-induced cardiomyocyte hypertrophy and apoptosis through the regulation of ubiquitination and activation of the NOTCH signaling pathway.","authors":"Jiarui Zhang, Wenwei Bai, Xiaoyong Liu, Jingjing Huang, Zhenxia Feng, Hu Li","doi":"10.1007/s10616-025-00763-1","DOIUrl":"10.1007/s10616-025-00763-1","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM), a cardiac condition resulting from diabetes, is linked to significant morbidity and mortality rates. TUBB4A, a variant of tubulin, is highly expressed in heart-related illnesses, yet its function in DCM remains unclear. In this study, 60 mg/kg streptozotocin (STZ) was intraperitoneally injected into mice to induce a diabetic model, and 30 mM glucose was added to H9C2 cell medium for 48 h to induce a high glucose (HG) cell model. In this study, TUBB4A expression was decreased in STZ- or HG-induced animal or cellular DCM models. The overexpression of TUBB4A diminished the effects of STZ or HG, enhanced the growth of myocardial cells, and prevented their hypertrophy and apoptosis. Moreover, it inhibited the expression of ROS, Bax and C-Caspase-3; promoted the expression of Bcl-2 and also alleviated DCM in vivo. Mechanistically, TUBB4A interacts with MYH9 and promotes NOTCH1 expression through MYH9-mediated deubiquitination, thereby inhibiting HG-induced cardiomyocyte hypertrophy and apoptosis and alleviating the development of DCM. Our study suggests that increasing TUBB4A expression may be a potential strategy for the treatment of DCM.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"100"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093155","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":"LncRNA OIP5-AS1 promotes immune evasion in abdominal aortic aneurysm cells by recruiting MDSCs and inhibiting CD8 + T cells through STK24 upregulation.","authors":"Baoping Deng, Qili Liu, Qingqing Xiao, Minjie Yang, Xiaoyong Ge, Jiacong Weng, Hongmei Zheng, Weiping Deng","doi":"10.1007/s10616-025-00767-x","DOIUrl":"10.1007/s10616-025-00767-x","url":null,"abstract":"<p><p>This study aims to investigate the expression and immune function of long non-coding RNA OIP5-AS1 (OIP5-AS1) and Serine/Threonine Kinase 24 (STK24) in abdominal aortic aneurysm (AAA). An animal model of AAA was established, along with cell models for overexpression and underexpression of OIP5-AS1 and STK24. Histological staining, qPCR, enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 assay, western blotting, RNA immunoprecipitation (RIP) analysis, and flow cytometry were employed to assess their effects on inflammation, cell proliferation, and apoptosis. In this study, Immunohistochemistry and qPCR analyses revealed significant upregulation of OIP5-AS1 and STK24 in both AAA tissue samples as well as cell models. ELISA demonstrated that elevated levels of OIP5-AS1 and STK24 significantly enhanced the secretion of inflammatory cytokines (IL-1β, IL-6, TNF-α, and IFN-γ), promoted cell proliferation while inhibiting apoptosis. RIP analysis combined with RNA pull-down assays indicated that OIP5-AS1 binds to the promoter region of STK24 by recruiting Zinc Finger Protein 93 (ZNF93) transcription factor leading to increased transcriptional expression of STK24. Furthermore, it was found that the functional role played by OIP5-AS1/STK24 axis operates through the AKT pathway. Increased expression levels of either OIP5-SAI or STK24 facilitated myeloid- derived suppressor cells (MDSCs) migration while suppressing CD8 + T-cell activity. The findings from this study highlight the critical involvement of the OIP5-SAI/STK24 axis in AAA progression by promoting MDSCs migration while inhibiting CD8 + T-cell activity. These insights provide novel perspectives into understanding the molecular pathology underlying AAA development while identifying potential therapeutic targets.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00767-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"102"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093149","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":"cPLA₂α on the influence of Th17 and its role in the formation of liver fibrosis.","authors":"Lina Ma, Wei Wang, Limin Gu, Liyun Wang","doi":"10.1007/s10616-025-00750-6","DOIUrl":"https://doi.org/10.1007/s10616-025-00750-6","url":null,"abstract":"<p><p>This study primarily investigated the mechanism and pathways of the cPLA₂α signaling pathway on Th17-mediated HSC activation and liver fibrosis, providing insights for clinical strategies to target HSC activation and delay the rapid progression of liver fibrosis. In vitro and in vivo model were established, and different concentrations of the cPLA₂α inhibitor AACOCF3 were administered respectively for intervention. The expression of IL- 17 was detected by ELISA, and the expression of cPLA₂α protein and HSC activation protein α-SMA index were detected by Western blot and immunofluorescence. In addition, observe the changes in the degree of liver fibrosis in mice through the pathological staining of mouse livers. In an in vitro system, Th17 could induce HSC activation. And after intervention, the results showed that the inhibitor could inhibit Th17 activation of HSC. Next, in an in vivo model, Th17 could also induce HSC activation. And after intervention, the results showed that the inhibitor could also inhibit HSC activation by Th17. Observation under liver pathological staining showed that the inflammation and staining were significantly reduced in the intervention group, suggesting a therapeutic effect of AACOCF3. Using in vitro and in vivo approaches, these data suggest that Th17 cells can promote the activation and proliferation of HSCs, which further exerts a role in promoting liver fibrosis. These data also suggest that the cPLA₂α pathway may be involved in the activation of HSCs by Th17 cells and induce liver fibrosis mechanisms.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"87"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes derived from human umbilical cord blood mesenchymal stem cells protect against blue light-induced damage to retinal pigment epithelial cells by inhibiting FGF2 expression.","authors":"Guang-Ming Liu, Yan Liu","doi":"10.1007/s10616-025-00752-4","DOIUrl":"https://doi.org/10.1007/s10616-025-00752-4","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is a debilitating retinal disorder that may lead to progressive vision loss. One contributing factor to AMD pathogenesis is excessive blue light (BL) exposure. In this study, we investigated the therapeutic potential of exosomes derived from human umbilical cord blood mesenchymal stem cells (hUCMSC-EXs) in addressing BL-induced damage to ARPE-19 human retinal pigment epithelial (RPE) cells and explored the underlying mechanisms. Our findings revealed that BL exposure induced morphological alterations in ARPE-19 cells, accompanied by a time-dependent decline in cell viability, increased apoptosis, heightened oxidative stress, and inflammatory responses; however, hUCMSC-EXs dose-dependently mitigated BL-induced ARPE-19 cell damage. Interestingly, hUCMSC-EXs were found to suppress the upregulation of fibroblast growth factor 2 (FGF2) in BL-exposed ARPE-19 cells. Furthermore, FGF2 overexpression partially counteracted the inhibitory effects of hUCMSC-EXs on FGF2 expression and compromised the protective benefits of hUCMSC-EXs against BL-induced ARPE-19 cell damage. In conclusion, our results suggest that hUCMSC-EXs shield ARPE-19 cells from BL-induced harm by inhibiting FGF2 expression.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"88"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of the N6-methyladenosine reader heterogeneous nuclear ribonucleoprotein C facilitating immune escape in thyroid cancer by stabilizing programmed death ligand 1.","authors":"Nuoxuan Li, Liang Wang, Jie Yao, Hong Yang","doi":"10.1007/s10616-025-00755-1","DOIUrl":"https://doi.org/10.1007/s10616-025-00755-1","url":null,"abstract":"<p><p>Thyroid cancer (TC) is a leading malignancy of the endocrine system. We investigated mechanism of the N6-methyladenosine (m6A) reader heterogeneous nuclear ribonucleoprotein C (HNRNPC) facilitating immune escape in TC by stabilizing programmed death ligand 1 (PD-L1). HNRNPC expression in TC tissues was analyzed using databases. Human TC cells (BHT-101, B-CPAP, SW579) and human thyroid follicular epithelial cells (Nthy-ori3-1) were cultured in vitro. SW579 cells were treated with pcDNA3.1-HNRNPC (oe-HNRNPC) and small interfering (si)-PD-L1, and B-CPAP cells were transfected with si-HNRNPC. HNRNPC and PD-L1 expression levels were assessed by RT-qPCR and Western blot. Cell proliferation, migration and invasion were evaluated by CCK-8, colony formation, and Transwell assays. Carboxyfluorescein diacetate succinimidyl ester-labelled CD8⁺ T cell proliferation and effector cytokine (interferon-γ, tumor necrosis factor-α) levels were measured by flow cytometry and ELISA. The correlation between HNRNPC and PD-L1 expression in TC tissues, m6A modification sites on PD-L1 messenger RNA (mRNA), and HNRNPC-PD-L1 interaction were analyzed by databases and RIP assay. PD-L1 m6A modification was determined by Me-RIP assay. PD-L1 mRNA stability was detected by treating cells with actinomycin D. HNRNPC was notably highly expressed in TC cells. HNRNPC promoted TC cell proliferation, migration and invasion, facilitating immune escape. Mechanistically, HNRNPC mediated m6A modification to strengthen PD-L1 mRNA stability and up-regulate PD-L1 expression. Moreover, knockdown of PD-L1 partially reversed the promotional effect of HNRNPC on immune escape in TC cells. HNRNPC bolstered PD-L1 stability and up-regulated PD-L1 expression through m6A modification, thus promoting immune escape in TC.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"96"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Icariside II inhibits gastric cancer progression by suppressing the Wnt/β-catenin signaling pathway.","authors":"Rongrong Dou, Xiaowei Zhu, Xinyun Liu, Jingjing Bao, Rongrong Jin, Guangyao Mao, Hong Yu, Yifei Liu","doi":"10.1007/s10616-025-00761-3","DOIUrl":"10.1007/s10616-025-00761-3","url":null,"abstract":"<p><p>Gastric cancer is one of the common malignant tumours in clinical practice with poor prognosis and high mortality. Icariside II is a single compound extracted from the traditional Chinese medicine <i>Epimedium brevicornu</i> Maxim, and it is also the main active ingredient of <i>Epimedium brevicornu</i> Maxim that exerts pharmacological effects. Studies have shown that Icariside II has anti-tumour activity, but its mechanism of action on gastric cancer cells is unclear. This study aims to analyze the impact of Icariside II on gastric cancer cells as well as on xenograft tumor models of gastric cancer, and to examine the potential molecular regulatory pathways. GES-1, a normal gastric cell line, and gastric cancer cell lines AGS and MGC803 were cultured to investigate the cytotoxic effects of Icariside II using the methylthiazolyldiphenyl-tetrazolium (MTT). Flow cytometry (FCM) was employed to measure the impact of Icariside II on the apoptosis levels of gastric cancer cells, while western blot analysis was used to examine the expression of apoptosis-related proteins and the Wnt/β-catenin signaling pathway. Subsequently, a xenograft tumor model was established and treated with Icariside II to observe changes in tumor volume and weight in the model mice. Finally, alterations in the expression of the Wnt/β-catenin signaling pathway were assessed through immunofluorescence (IF) and immunohistochemistry (IHC). The results showed that Icariside II had faint significant toxic effect on GES-1 cells, and was able to inhibit the proliferative activity and promote apoptosis of the gastric cancer cells. Moreover, Icariside II was able to inhibit the growth of gastric cancer in nude mice subcutaneous transplantation tumor. In addition, both in vivo and in vitro results indicated that Icariside II inhibited the activation of the Wnt/β-catenin signaling pathway. Icariside II inhibited tumorigenicity of gastric cancer by suppressing the Wnt/β-catenin signaling.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"106"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12098252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141789","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}