Cell Biochemistry and Biophysics最新文献_第2页

FABP4 Downregulated by FOS Alleviates Palmitic Acid-induced Endothelial Cell Dysfunction Via Inactivating ERK/STAT-1 Signaling Pathway. FOS下调FABP4通过失活ERK/STAT-1信号通路缓解棕榈酸诱导的内皮细胞功能障碍

IF 2.5 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-28 DOI: 10.1007/s12013-025-01782-7

Mengting Ruan, Jin Zhang

{"title":"FABP4 Downregulated by FOS Alleviates Palmitic Acid-induced Endothelial Cell Dysfunction Via Inactivating ERK/STAT-1 Signaling Pathway.","authors":"Mengting Ruan, Jin Zhang","doi":"10.1007/s12013-025-01782-7","DOIUrl":"https://doi.org/10.1007/s12013-025-01782-7","url":null,"abstract":"This study aimed to explore the role and the mechanism of FABP4 in the pathogenesis of preeclampsia (PE). FABP4 expression in the whole blood and the placental tissue of PE patients and healthy pregnant women was detected using RT-qPCR. The transfection efficacy of sh-FABP4, sh-FOS and Ov-FOS was examined using Western blotting and RT-qPCR. CCK-8 assay was used to detect cell viability. TUNEL assay was used to detect cell apoptotic level. Wound healing and transwell assays were used to detect the migration and invasion of HUVECs. Tube formation assay was used to detect HUVEC s' angiogenic ability. Western blotting was used to measure the expressions of apoptosis- and ERK/STAT-1 signaling pathway-related proteins. Luciferase reporter assay was used to detect FABP4 promoter activity, while ChIP assay confirmed the binding ability of FOS to FABP4. FABP4 expression was increased in the whole blood and the placental tissue of PE patients and palmitic acid (PA)-treated HUVECs. FABP4 interference inhibited apoptosis while promoting the migration, invasion, and angiogenesis in PA-induced HUVECs via inactivating ERK/STAT-1. It was also identified that FOS reduced FABP4 activity and inhibited FABP4/ERK/STAT-1 signaling pathway. FABP4 protected against PA-induced endothelial cell dysfunction via the inhibition of ERK/STAT-1, which might be mediated by FOS.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Redox Signaling Disruption and Antioxidants in Toxicology: From Precision Therapy to Potential Hazards. 毒理学中的氧化还原信号中断和抗氧化剂：从精确治疗到潜在危害。

IF 2.5 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-28 DOI: 10.1007/s12013-025-01846-8

Esther Ugo Alum, Daniel Ejim Uti, Christian Emeka Offor

{"title":"Redox Signaling Disruption and Antioxidants in Toxicology: From Precision Therapy to Potential Hazards.","authors":"Esther Ugo Alum, Daniel Ejim Uti, Christian Emeka Offor","doi":"10.1007/s12013-025-01846-8","DOIUrl":"https://doi.org/10.1007/s12013-025-01846-8","url":null,"abstract":"Antioxidants play a vital role in neutralizing oxidative stress and maintaining cellular homeostasis. However, emerging evidence highlights their paradoxical nature, while beneficial in regulated doses, excessive or inappropriate supplementation may contribute to disease progression, chemoresistance, and redox signaling disruption. This narrative review examines both the protective and potentially harmful roles of antioxidants in toxicology, with a focus on therapeutic challenges and clinical implications. We reviewed relevant peer-reviewed articles, preclinical and clinical studies, and systematic reviews published between 2012 and 2024, using databases such as Scopus, Web of Science, and PubMed. Key findings indicate that antioxidants can inadvertently promote cancer progression under certain conditions, complicate treatment outcomes, and interfere with endogenous redox balance. The review explores precision medicine approaches for tailoring antioxidant therapy, as well as their effects on chronic diseases such as neurodegeneration and cardiovascular disorders. Further, we assess the role of antioxidants in mitigating oxidative damage induced by environmental toxicants like heavy metals and air pollutants. Innovative strategies, including nanotechnology-based delivery systems, are discussed as promising tools to enhance therapeutic specificity and minimize off-target effects. Overall, this review underscores the importance of understanding the nuanced role of antioxidants in toxicology to ensure their safe and effective clinical use, and it outlines critical directions.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Luteolin Inhibits Ferroptosis of HUVEC by Regulating the Sirt1/Nrf2 Pathway. 木犀草素通过调节Sirt1/Nrf2通路抑制HUVEC铁凋亡。

IF 2.5 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-28 DOI: 10.1007/s12013-025-01831-1

Ming Xiang, Xiangdong Lin, Haiying Chen

{"title":"Luteolin Inhibits Ferroptosis of HUVEC by Regulating the Sirt1/Nrf2 Pathway.","authors":"Ming Xiang, Xiangdong Lin, Haiying Chen","doi":"10.1007/s12013-025-01831-1","DOIUrl":"https://doi.org/10.1007/s12013-025-01831-1","url":null,"abstract":"Coronary heart disease (CHD) is a disease caused by organic and functional coronary artery stenosis, resulting in a reduced oxygen supply to the heart. This study aimed to investigate the mechanism via which Luteolin regulates the Sirt1/Nrf2 pathway to inhibit ferroptosis in human umbilical vein endothelial cells (HUVEC) associated with CHD. An ox-LDL-induced HUVEC cell model with Sirt1 silencing and Luteolin treatment was established. The silencing efficiency of Sirt1 was validated using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The results of molecular docking and DARTS experiments showed that Luteolin could effectively bind Sirt1. Subsequently, we measured the expression of Nrf2 and Sirt1, cell viability, MDA, GSH, Fe2+ levels, lipid ROS content, expression of ferroptosis-related proteins GPX4, FTH, FTL, and cell migration parameters. The results showed that Luteolin could activate the Sirt1/Nrf2 axis and effectively inhibit ox-LDL-induced ferroptosis in HUVEC. Experimental results revealed that Luteolin could enhance HUVEC cell viability, decrease MDA, Fe2+, and ROS levels, increase GSH levels, promote the expression of HO-1, GPX4, FTH, FTL, inhibit the expression of ACSL4 and TFRC, and enhance the migration capability of HUVEC cells. Moreover, silencing Sirt1 reversed the effects of Luteolin on the activation of Sirt1 and Nrf2, confirming the dependence of these effects on the Sirt1/Nrf2 signaling pathway. In conclusion, this study indicates that Luteolin could inhibit ferroptosis in HUVEC in CHD by modulating the Sirt1/Nrf2 axis, providing a basis for further research on strategies for preventing and treating CHD and related diseases.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential of Amaranthus tricolor Terpenoids in Managing Obesity by Modulating the PI3K/AKT Pathway: A Network Pharmacology Approach. 三色苋萜类化合物通过调节PI3K/AKT通路控制肥胖的潜力：网络药理学方法。

IF 2.5 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-28 DOI: 10.1007/s12013-025-01842-y

Aditya Khandelwal, Bhamini Pande, Jyotsana, Promila Gupta

{"title":"Potential of Amaranthus tricolor Terpenoids in Managing Obesity by Modulating the PI3K/AKT Pathway: A Network Pharmacology Approach.","authors":"Aditya Khandelwal, Bhamini Pande, Jyotsana, Promila Gupta","doi":"10.1007/s12013-025-01842-y","DOIUrl":"https://doi.org/10.1007/s12013-025-01842-y","url":null,"abstract":"Obesity is a condition where disproportionate body fat accumulation, leads to adverse health issues. Amaranthus tricolor is a popularly consumed leafy vegetable with reported therapeutic effects, including anti-inflammatory and hepatoprotective activities. Presently, the potential of terpenoids identified in the leaf extracts of A. tricolor was explored to manage obesity. Initially, the Total Terpenoid Content (TTC) and antioxidant potential of the hexane extract (HE) and methanolic extract (ME) was explored. Since, HE displayed better terpenoid content and antioxidant potential, its Gas Chromatography-Mass Spectrometry (GC-MS) chromatogram was used to identify and shortlist the terpenoids (1,2-15,16-Diepoxyhexadecane, α-tocopherol, Chondrillasterol, γ-tocopherol, Neophytadiene, Phytol and Squalene) present in it for in silico analysis. Network Pharmacology approach was utilised to identify hub genes (AKT1, HSP90AA1, PIK3CA, and SRC) of the shortlisted terpenoids. Molecular docking and simulation studies of the hub genes was performed using AutoDock Vina and GROMACS. α-tocopherol, Chondrillasterol and γ-tocopherol were shortlisted as the most promising terpenoids with potential to manage obesity by modulating the PI3K/AKT pathway. The current study highlighted the potential of terpenoids present in A.tricolor to alleviate obesity and provided strong theoretical indications to develop therapeutic interventions using such compounds.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunomodulatory Activity of Propafenone Hydrochloride on Mammalian Macrophages in the Presence of LPS. 盐酸普罗帕酮在LPS作用下对哺乳动物巨噬细胞的免疫调节作用。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-25 DOI: 10.1007/s12013-025-01800-8

Tanya Beril Korkmaz, Hülya Servi, Furkan Ayaz

{"title":"Immunomodulatory Activity of Propafenone Hydrochloride on Mammalian Macrophages in the Presence of LPS.","authors":"Tanya Beril Korkmaz, Hülya Servi, Furkan Ayaz","doi":"10.1007/s12013-025-01800-8","DOIUrl":"https://doi.org/10.1007/s12013-025-01800-8","url":null,"abstract":"Propafenone is an antiarrhythmic medication with the properties that span both class 1 and class 2 antiarrhythmic drugs. It regulates the heart rhythm through the blockage of sodium channel, potassium channel, and beta receptors. In the literature, there are studies related to the effects of Propafenone on atrial fibrillation, as well as its potential anti-cancer and anti-epileptic effects. However, there is currently insufficient research on Propafenone's immunomodulatory effects. In this study, the immunomodulatory activity of propafenone was tested. Impact of Propafenone on TNF-α, IL-6, Il-12p40 and GM-CSF cytokines production by J774.2 macrophage cell line was evaluated in the presence and absence of LPS (lipopolysaccharide). Cytokine production level was tested in the presence of propafenone. The results showed that Propafenone alone did not significantly stimulate cytokine release, but in the presence of LPS, it showed a significant effect and demonstrated anti-inflammatory activity. Propafenone has anti-inflammatory activity. At the clinical setting this information should be taken into the consideration if anti-inflammatory drug utilization is also necessary to prevent extra usage of the drug molecules. In case of infections, the patients who are using propafenone should get immune boosting supplements to be able to cope with the infectious agent.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In Silico Evaluation of Acalypha indica Phytochemicals as Potential Antifungal Agents Targeting Saccharomyces cerevisiae Lanosterol 14-Alpha Demethylase. 猕猴桃植物化学物质作为酿酒酵母菌羊毛甾醇14- α去甲基化酶潜在抗真菌药物的硅片评价

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-22 DOI: 10.1007/s12013-025-01836-w

Mic Arun Edwin, Ramaiyan Velmurugan, Saraswati Patel

{"title":"In Silico Evaluation of Acalypha indica Phytochemicals as Potential Antifungal Agents Targeting Saccharomyces cerevisiae Lanosterol 14-Alpha Demethylase.","authors":"Mic Arun Edwin, Ramaiyan Velmurugan, Saraswati Patel","doi":"10.1007/s12013-025-01836-w","DOIUrl":"https://doi.org/10.1007/s12013-025-01836-w","url":null,"abstract":"The rise in antifungal resistance underscores the need to explore novel bioactive compounds. This study investigates phytochemicals from Acalypha indica as potential inhibitors of lanosterol 14-alpha demethylase (CYP51) in Saccharomyces cerevisiae. A total of sixteen phytocompounds were evaluated using molecular docking, MM/GBSA binding free energy estimation, pharmacokinetic and toxicity predictions, and 200 ns molecular dynamics (MD) simulations. Among them, stigmasterol, aurantiamide, and beta-sitosterol showed strong binding affinities, comparable to standard drugs fluconazole and itraconazole. ADME analysis revealed good drug-likeness and gastrointestinal absorption for aurantiamide and 2-methylanthraquinone. ProTox-III predictions indicated low mutagenic and carcinogenic risks for most compounds, although aurantiamide may have nephrotoxic and respiratory toxicity concerns. Top ligands aurantiamide and stigmasterol were further subjected to MD simulations, which demonstrated stable RMSD, low RMSF, and well-maintained secondary structure, indicating strong interaction persistence and structural integrity. Ligand behaviour metrics (rGyr, SASA, MolSA, PSA, intra-HB) supported their binding stability. While aurantiamide exhibited an unfavourable binding energy (+228.37 kcal/mol), stigmasterol displayed a significantly favourable ΔG_bind (-93.36 kcal/mol). These findings suggest that stigmasterol and related phytochemicals hold promise as natural antifungal agents. However, further in vitro and in vivo validation, along with structure-activity relationship (SAR) optimization, is essential for clinical advancement.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144688493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pathological Changes in Liver Mitochondria of Rats with Experimentally Induced Hyperthyroidism and Their Correction with Uridine. 实验性甲状腺机能亢进大鼠肝脏线粒体的病理改变及尿苷的纠正作用。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-22 DOI: 10.1007/s12013-025-01838-8

Natalya Venediktova, Natalya Khmil, Lyubov Pavlik, Irina Mikheeva, Galina Mironova

引用次数: 0

Thiamine Mitigates the Toxicity of Methylmercury in Cultured Fetal Fibroblast Cell Lines. 硫胺素减轻甲基汞对培养的胎儿成纤维细胞系的毒性。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-21 DOI: 10.1007/s12013-025-01841-z

Parisa Sadighara, Jamileh Salar-Amoli, Abbas Barin, Sher Ali, Carlos Augusto Fernandes Oliveira

{"title":"Thiamine Mitigates the Toxicity of Methylmercury in Cultured Fetal Fibroblast Cell Lines.","authors":"Parisa Sadighara, Jamileh Salar-Amoli, Abbas Barin, Sher Ali, Carlos Augusto Fernandes Oliveira","doi":"10.1007/s12013-025-01841-z","DOIUrl":"https://doi.org/10.1007/s12013-025-01841-z","url":null,"abstract":"The challenge in addressing methylmercury (MeHg) poisoning primarily lies in devising effective therapeutic strategies. In this study, we explore the potential cytoprotective effects of thiamine pyrophosphate (TPP) as a novel agent to alleviate MeHg-induced complications. Fetal fibroblast cells were exposed to 100 µM MeHg with varying concentrations of TPP (12.5-100 mM). Treated and control cells were analyzed for determination of DNA and protein contents, whereas glutathione and lipid peroxidation levels were measured as oxidative stress markers. TPP reduced the cellular lipid peroxidation and restored the intracellular glutathione levels altered by MeHg, also increasing the cell DNA content in the 12.5 mM TPP treatment group. TPP treatment led to enhanced cell survival, underscoring TPP's capacity to alleviate MeHg toxicity by improving the antioxidant status. Further studies on additional oxidative stress markers and apoptotic pathways are necessary to fully elucidate the scope and mechanisms of TPP's cytoprotective effects against MeHg toxicity. While the data in this trial highlight the potential of TPP as a novel therapeutic agent for individuals exposed to MeHg, clinical studies are required to confirm its protective efficacy aiming at developing future mitigation strategies.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of Metformin Treatment Against Endometrial Cancer Cells Cultured In Vitro or Grafted into Female Balb/C Nude Mice: Insights into Cell Response and IGF-1R and PI3K/AKT/mTOR Signaling Pathways. 二甲双胍治疗对体外培养或移植到雌性Balb/C裸鼠子宫内膜癌细胞的影响：细胞反应和IGF-1R和PI3K/AKT/mTOR信号通路的见解

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-21 DOI: 10.1007/s12013-025-01840-0

Vânia Marísia Santos Fortes Dos Reis, Franciely Machado Ramos, Henrique Leal de Oliveira, Fernanda Dapper Machado, Sara Hartke, Amanda Machado-Weber, Ariane Germeyer, Thomas Strowitzki, Lúcia Maria Kliemann, Helena von Eye Corleta, Ilma Simoni Brum, Edison Capp, Leo Anderson Meira Martins

{"title":"Effects of Metformin Treatment Against Endometrial Cancer Cells Cultured In Vitro or Grafted into Female Balb/C Nude Mice: Insights into Cell Response and IGF-1R and PI3K/AKT/mTOR Signaling Pathways.","authors":"Vânia Marísia Santos Fortes Dos Reis, Franciely Machado Ramos, Henrique Leal de Oliveira, Fernanda Dapper Machado, Sara Hartke, Amanda Machado-Weber, Ariane Germeyer, Thomas Strowitzki, Lúcia Maria Kliemann, Helena von Eye Corleta, Ilma Simoni Brum, Edison Capp, Leo Anderson Meira Martins","doi":"10.1007/s12013-025-01840-0","DOIUrl":"https://doi.org/10.1007/s12013-025-01840-0","url":null,"abstract":"Obesity and type II diabetes are independent risk factors for Endometrial cancer (EC) development. Elevated levels of insulin-like growth factor-1 (IGF-1), insulin resistance, and the increased activity of IGF-1 receptor is linked to EC development through the PI3K/AKT/mTOR pathway. The antidiabetic agent metformin is a promising repurposing drug for cancer treatment, but the mechanisms underlying its effects are not completely known. This study evaluated how metformin could act against the EC cell line Ishikawa cultured in vitro or grafted into female Balb/C nude mice. In vitro experiments demonstrated that treatment with 25 mM of metformin reduced cell viability through promoting cytotoxicity, mitochondrial dysfunction, apoptosis, and cell cycle arrest (G1 phase). Mice treatment with 250 mg/kg of metformin for 28 days did not change serum IGF-1 levels nor decreased the grafted cell-induced tumor weight and cell proliferation, but prevented its volume growth while genes of the IGF1-R and PI3K/AKT/mTOR pathways (AKT2, GAPDH, FOXO3, IGF1R, INSR, MAPK3, MTOR, and SHC1) were downregulated. Metformin treatment was more impacting for the in vitro model, but our molecular results provide valuable insights into the possible action of metformin against EC tumoral cells at physiological level. In-silico analysis using Cytoscape indicated that metformin was not described as interacting with AKT2 and SHC1 proteins. Besides interacting with metformin, mTOR and MAPK3 present the larger number of interactions with the other proteins. These four genes/proteins emerge as potential targets for deepening studies to determine the metformin's role in longer EC treatment using animal models.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Royal Jelly Enhances the Sensitivity of Oral Squamous Cancer Cells to Paclitaxel, Suppressing Proliferation, Migration, and Glycolysis. 蜂王浆增强口腔鳞癌细胞对紫杉醇的敏感性，抑制增殖、迁移和糖酵解。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-07-19 DOI: 10.1007/s12013-025-01834-y

Tuğba Kul Köprülü, Bahar Gezer, Jülide Balkan

{"title":"Royal Jelly Enhances the Sensitivity of Oral Squamous Cancer Cells to Paclitaxel, Suppressing Proliferation, Migration, and Glycolysis.","authors":"Tuğba Kul Köprülü, Bahar Gezer, Jülide Balkan","doi":"10.1007/s12013-025-01834-y","DOIUrl":"https://doi.org/10.1007/s12013-025-01834-y","url":null,"abstract":"Royal jelly (RJ) is a natural product that reduces toxic effects and has anti-proliferative effects. The aim of the study is to increase the anticancer effect of Paclitaxel (PAX), which is used in cancer treatment, and to reduce its toxic effect with RJ in oral squamous carcinoma cells. Cytotoxicity tests of RJ and PAX substances were tested on healthy gingival HGF cells and their anti-proliferative effects on UPCI-SCC-131 cells with real-time cell analyzer (xCELLigence RTCA). Their anti-migratory properties were observed with wound healing assay. Glycolysis stress test was performed with Seahorse XFe24 to measure the glycolytic capacity. Total RNA-seq libraries were created and sequenced with NovaSeq 6000. Transcriptome profiles were created with bioinformatic analyses and functional enrichment analyses were performed. Results demonstrate that both RJ and PAX exhibit significant anti-proliferative effects against oral squamous cell carcinoma cells, as quantified by real-time cell analysis. Notably, RJ co-treatment mitigated PAX-induced cytotoxicity in healthy human gingival fibroblasts, suggesting a protective role against chemotherapy-associated toxicity. While both compounds inhibited cancer cell proliferation, PAX particularly displayed potent anti-migratory properties in wound healing assays, significantly impairing OSCC cell motility. Metabolic profiling revealed that the RJ-PAX combination therapy substantially reduced glycolytic capacity in OSCC cells, indicating disruption of their energy metabolism. Transcriptomic analysis identified downregulation of critical cell cycle regulators (MCM2, CDC25A, CCNE2) and DNA replication factors (RFC2, PCNA), along with modulation of MYC and E2F pathways, providing insights into the observed anti-cancer effects.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0