Human & experimental toxicology最新文献

{"title":"Dexmedetomidine and propofol-induced neurotoxicity: Promise, but caution warranted.","authors":"Mohamed Yasser El-Mezayen, Marwa Farouk, Bothaina Farouk, Mariam El-Mezayen, Sahar Eissa","doi":"10.1177/09603271251387257","DOIUrl":"https://doi.org/10.1177/09603271251387257","url":null,"abstract":"","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251387257"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of SIRT3/AMPK/mTOR-mediated autophagy promotes quercetin-induced ferroptosis in oral squamous cell carcinoma.","authors":"Jin Wang, Jia-Hui Yang, Di Xiong, Ling Chen","doi":"10.1177/09603271251323753","DOIUrl":"10.1177/09603271251323753","url":null,"abstract":"<p><strong>Introduction: </strong>Quercetin has been reported to inhibit the growth of oral squamous cell carcinoma (OSCC), but the mechanism remains unclear. Therefore, our study aimed to investigate the involvement of sirtuin 3 (SIRT3) and the autophagy-dependent form of cell death, ferroptosis, in the pathogenesis of OSCC, and observe the impacts of quercetin on ferroptosis and SIRT3/AMPK/mTOR-mediated autophagy.</p><p><strong>Methods: </strong>SIRT3 knock out or overexpressing SCC15 cell line was generated, treated with indicated drugs, and malondialdehyde (MDA) and ROS levels were measured. Roles of SIRT3 in regulating autophagy-mediated ferroptosis were assessed by immunoprecipitation and Western blotting.</p><p><strong>Results: </strong>SIRT3 overexpression increased levels of MDA and ROS, reducing cell viability, and SIRT3 knockout produced the opposing effect. SIRT3 overexpression upregulated ATG16L1 expression and the conversion of LC3-Ⅰ to LC3-Ⅱ, triggering autophagy. Suppression of autophagy by ATG16L1 knockout impaired SIRT3-triggered ferroptosis. Use of an AMPK inhibitor antagonized the induction of ferroptosis by SIRT3 in SCC15 cells, indicating the involvement of the AMPK/mTOR pathway. Additionally, quercetin significantly increased the levels of SIRT3, p-AMPK, ATG16L1, and the ratio of LC3-Ⅱ/Ⅰ, but reduced cell viability and p-mTOR in SCC15 cells. Autophagy and AMPK inhibitors, or SIRT3 deletion significantly antagonized the impacts of quercetin on the autophagy-mediated ferroptosis in cancer cells.</p><p><strong>Discussion: </strong>SIRT3 overexpression activated the AMPK/mTOR pathway and triggered ATG16L1-mediated autophagy, promoting ferroptosis in SCC15 cells, and we proposed that quercetin may be a promising therapeutic drug for OSCC.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251323753"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pelargonidin-3-O-glucoside prevents isoproterenol-induced myocardial infarction via modulating cardiac and inflammatory markers expression in experimental rats.","authors":"Jianmei Chang, Xiaoling Guo, Peng Hou","doi":"10.1177/09603271251369054","DOIUrl":"https://doi.org/10.1177/09603271251369054","url":null,"abstract":"<p><p>IntroductionThis study examined the cardioprotective effects of Pelargonidin-3-O-glucoside (Pg3G) against myocardial infarction induced by isoproterenol (ISO) in male Wistar rats.MethodsAnimals were divided into four groups each groups contain six animals. Group 1 control; Group 2 Pg3G treated control; Group 3 ISO-control; Group 4 Pg3G + ISO treated rats. At the end of the experiment period the animals were sacrificed and collected the serum, heart tissue used for the experimental work.ResultsAccording to the network pharmacology analysis, Prostaglandin-endoperoxide Synthase 2 (PTGS2), Matrix metallo proteins -9 (MMP-9), and tumour necrosis factor-alpha (TNF-α) were identified as potential targets among the 97 common targets between Pg3G and myocardial injury. Further, we investigated that prominent cardiac indicator such creatine kinase (CK), CK-MB, cardiac troponin T (cTnT), and cardiac troponin I (cTnI) were not elevated by ISO in the presence of Pg3G administration. Additionally, Pg3G administration decreased the pro-inflammatory cytokines generated by ISO, including as interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and TNF-α, suggesting its anti-inflammatory qualities. Additionally, Pg3G increased levels of reduced glutathione (GSH) and restored the activity of important antioxidant enzymes that were depleted by ISO-induced oxidative stress, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD).DiscussionPg3G capacity to reduce ISO-induced inflammatory, fibrotic, and cardiac toxicity markers in myocardial tissue was demonstrated by gene expression investigations. Therefore, Pg3G may be considered for ISO-induced cardiac injury since it provides significant cardioprotection by reducing oxidative stress, inflammation, and fibrosis.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251369054"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144983971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of <i>Tribulus Terrestris</i> extract on cisplatin-induced ovarian damage: Antioxidants and anti-inflammatory insights.","authors":"Morteza Abdi, Hadi Karimzadeh, Amirreza Jourabchi, Abbas Majdi Seghinsara, Laleh Khodaie","doi":"10.1177/09603271251353492","DOIUrl":"https://doi.org/10.1177/09603271251353492","url":null,"abstract":"<p><p>BackgroundCisplatin (CIS) is a widely used chemotherapeutic agent; however, it is associated with ovarian toxicity. <i>Tribulus Terrestris</i> (TT) is recognized for its antioxidant and anti-inflammatory properties. This study aims to evaluate the effects of TT extract on ovarian tissue damage induced by cisplatin.Material and MethodTwenty-five female BALB/c mice were divided into five groups (n = 5): Control, CIS (Cisplatin only), CIS + TT100 (100 mg/kg TT extract daily + CIS), CIS + TT300 (300 mg/kg TT + CIS), and CIS + TT500 (500 mg/kg TT daily + CIS). After 15 days, blood samples were collected for hormonal analysis, and ovaries were harvested for histopathological, immunohistochemical, and biochemical assessments.ResultsThe CIS group exhibited a significant decline in follicle count compared to the control group (P < 0.001). In contrast, the CIS + TT groups showed a notable increase in follicle count (P < 0.05). TT treatment also resulted in significant improvements in antioxidant markers (SOD, CAT) and a reduction in oxidative stress (MDA) compared to the CIS group. Moreover, E2, AMH, and progesterone concentrations were decreased in the CIS group, while these levels were restored in the TT-treated groups (P < 0.001). The expression of inflammatory markers TNF-α and IL-1β was higher in the CIS group and decreased in the TT-treated groups.Conclusion<i>Tribulus Terrestris</i> extract effectively mitigates cisplatin-induced ovarian toxicity by enhancing follicular count, improving antioxidant activity, and reducing oxidative stress. TT treatment also elevated AMH and progesterone levels while decreasing inflammatory markers, underscoring its potential as a protective agent against cisplatin-induced ovarian damage.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251353492"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of detergent component sodium dodecyl sulfate on growth hormone secretion in GH3 cells: Implications for pediatric exposure and accidental ingestion.","authors":"Hua Tang, Lanlan Li","doi":"10.1177/09603271251332255","DOIUrl":"10.1177/09603271251332255","url":null,"abstract":"<p><p>IntroductionSodium dodecyl sulfate (SDS), a widely used surfactant in detergents, has raised concerns due to its potential health risks, particularly in children. This study evaluates the impact of SDS exposure on GH secretion in GH3 cells, focusing on oxidative stress as a key mechanism.MethodsGH3 cells were treated with varying concentrations of SDS (0.001-10 mM) for 24 or 48 h. Cell viability was assessed using the MTT assay, while GH secretion was quantified via ELISA. Oxidative stress levels were evaluated through ROS fluorescence assays, and gene expression of Nrf2, IL-6, TNF-α, and caspase-3 was analyzed using qPCR. Additionally, the antioxidant N-acetylcysteine (NAC) was used to determine its protective effects against SDS-induced oxidative stress.ResultsSDS exposure led to a dose-dependent decrease in GH secretion and cell viability, with oxidative stress identified as a primary driver. Nrf2 exhibited a biphasic response, showing transient upregulation at low doses but suppression at higher concentrations, exacerbating oxidative damage. NAC treatment reduced ROS levels and partially restored GH secretion, confirming the role of oxidative stress in SDS-induced toxicity.DiscussionThese findings suggest that SDS exposure may disrupt endocrine function, warranting further risk assessment of its safety in consumer products. Given SDS's prevalence in household products, future research should focus on the long-term effects of SDS exposure to children and potential therapeutic interventions to mitigate oxidative damage.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332255"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In silico and in vivo experiments of Huperzine A modulating the development of obstructive sleep apnea by transcriptionally regulating pyruvate carboxylase expression via retinoid X receptor alpha.","authors":"Juan Huang, Hui Li, Qin Huang, Li Wang, Ying Wu, Xin Tan","doi":"10.1177/09603271251342572","DOIUrl":"https://doi.org/10.1177/09603271251342572","url":null,"abstract":"<p><p>IntroductionThis study investigated the molecular mechanism by which HuA influences the expression of pyruvate carboxylase via retinoid X receptor alpha (RXRA), thereby affecting the progression of obstructive sleep apnea (OSA).MethodsBioinformatics analysis including screening of differentially expressed genes (DEGs) and searching the downstream target genes of RXRA were conducted. Cognitive function, neuronal damage, oxidative stress, and inflammation were evaluated in chronic intermittent hypoxia (CIH) mouse models. The Morris water maze test was used to assess swimming path length, escape latency, and platform crossing times. H&E and Nissl staining was performed to evaluate pathological changes and neuronal counts in brain tissue. ELISA was utilized to measure the oxidative stress levels and inflammatory cytokines. RXRA enrichment in the pyruvate carboxylase promoter region in CIH was assessed using Chromatin Immunoprecipitation (ChIP), and the effect of RXRA on pyruvate carboxylase promoter activity was analyzed using dual-luciferase assay.ResultsRXRA was identified as a potential regulatory target gene of HuA. Pyruvate carboxylase was identified as a RXRA target gene and a significant DEG in OSA. CIH-induced cognitive impairment, neuronal damage, oxidative stress, and inflammation in mice, while such symptoms were alleviated by HuA treatment. In OSA, suppression of RXRA expression led to reduced pyruvate carboxylase expression. HuA treatment enhanced RXRA expression, thereby promoting pyruvate carboxylase expression. HuA alleviated CIH-induced cognitive impairment, neuronal damage, oxidative stress, and inflammation via the RXRA/pyruvate carboxylase axis.ConclusionIn summary, HuA alleviates CIH-induced cognitive impairment, neuronal damage, oxidative stress, and inflammation by promoting the RXRA/pyruvate carboxylase axis.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251342572"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cigarette smoking extract induces mitochondrial dysfunction and apoptosis in HUVECs via the Sirt1-SHH axis.","authors":"Weiming Wang, Gang Yuan, Guang Li, Tingting Zhao, Yue Chen, Youhua Xu","doi":"10.1177/09603271251332251","DOIUrl":"10.1177/09603271251332251","url":null,"abstract":"<p><p>IntroductionCigarette smoking extract (CSE) can cause endothelial cell (EC) dysfunction, and then promote the occurrence and development of atherosclerosis. However, the molecular mechanisms underlying CSE-induced EC dysfunction are unknown. Sirt1, as a deacetylase, is involved in various biological processes of ECs. Therefore, this study investigated whether CSE induces apoptosis and mitochondrial dysfunction in human umbilical vein endothelial cells (HUVECs) via Sirt1-dependent mechanisms.MethodsHUVEC activity was assessed using MTT and crystal violet staining following treatment with different concentrations of CSE. Lentiviral transfection technology was used to generate HUVECs overexpressing Sirt1. Apoptosis was detected by Tunnel staining. MitoTracker™ Deep Red FM and JC-1 were used to assess mitochondrial structure and membrane potential. ELISA was used to detect the expression of superoxide dismutase (SOD) and malondialdehyde (MDA). qPCR was used to determine mRNA expression. Atherosclerosis was evaluated by oil red O staining in ApoE-KO mice after cigarette smoke exposure.ResultsCSE decreased Sirt1 and sonic hedgehog (SHH) expression, leading to mitochondrial dysfunction and apoptosis in HUVECs. Overexpressing Sirt1 or activating the SHH signaling pathway attenuated CSE-induced apoptosis and mitochondrial dysfunction. However, inhibiting the SHH signaling axis attenuated the protective effect of Sirt1 overexpression on CSE-induced apoptosis and mitochondrial dysfunction. In vivo studies also showed that cigarette smoke exacerbated atherosclerosis in ApoE-KO mice, downregulating Sirt1, SHH, and Gli1 expression in the aorta. Additionally, cigarette smoke increased Bax expression and decreased Bcl-2 expression in ApoE-KO mice aortas.DiscussionsSmoking can affect all stages of the atherosclerosis process, and the specific mechanism remains unclear. This study confirms that CSE can induce mitochondrial dysfunction and apoptosis of HUVECs by reducing Sirt1 expression and inhibiting SHH signaling activation. These findings provide new insights into the prevention and treatment of smoking-induced atherosclerosis.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332251"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network pharmacology and experimental verification: Rosmarinic acid alleviates doxorubicin-induced cardiomyocyte apoptosis by regulating BCL2L1.","authors":"Sicong Xie, Cheng Chang, Rongxing Jiang, Lifeng Wang, Yunli Yang, Zongjin Li, Yang Zhang","doi":"10.1177/09603271251354890","DOIUrl":"https://doi.org/10.1177/09603271251354890","url":null,"abstract":"<p><p>PurposeThis study investigated the mechanism by which Rosmarinic acid (RA) may alleviate doxorubicin (DOX)- induced cardiomyocyte apoptosis.MethodsThe target genes of RA, DOX-related differentially expressed genes, and GEO database related genes were retrieved by bioinformatics analyses. The results of these analyses were further intersected to identify candidate genes. The protein-protein interaction network was constructed to develop the pharmacophore model. The molecular docking was simulated to determine the core target B-cell lymphoma 2-like 1 (BCL2L1) for subsequent molecular mechanism investigation <i>in vitro</i>. The effects of DOX and RA on the apoptosis of H9c2 cells were assessed using the CCK8 assay. The present study investigated the effect of RA on DOX-induced oxidative stress in cardiomyocytes. This investigation was conducted using an ELISA test and a DCFH-DA probe. The JC-1 probe was utilized to assess the effect of RA on DOX-induced cardiomyocyte mitochondrial membrane permeability. A Western blot assay was conducted to ascertain the activation of multiple signaling molecules, including those belonging to the BCL-2 and caspase-3 families, within the apoptosis pathway.ResultsA total of 17 differentially expressed genes (DEGs) were screened, and five genes were selected as hub DEGs. A subsequent KEGG enrichment analysis revealed that these DEGs were significantly enriched in various biological processes and pathways, including the MAPK signaling pathway, autophagy, apoptosis, and the TNF signaling pathway. The pharmacophore model and molecular docking of five candidate targets with RA were successfully established. It is noteworthy that DOX treatment led to a suppression of SOD and GSH levels, an exacerbation of oxidative stress, and a promotion of cardiomyocyte apoptosis. Furthermore, it has been demonstrated to suppress mitochondrial membrane permeability. Subsequent RT-qPCR analysis of the hub genes revealed that only <i>BCL2L1</i> exhibited significant alterations. Treatment with DOX altered the expression levels of apoptosis-associated proteins, BCL-2 family members, and caspase-3 family members. However, the administration of RA mitigated the deleterious effects of DOX on cardiomyocytes.ConclusionsThe protective effects of RA may against myocardial cell apoptosis are likely mediated through its activation of BCL2L1 and inhibition of caspase cascade protein expression in myocardial cells.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251354890"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into therapeutic potential and practical applications of natural toxins from poisonous mushrooms.","authors":"Tharuka Wijesekara, Baojun Xu","doi":"10.1177/09603271251323134","DOIUrl":"10.1177/09603271251323134","url":null,"abstract":"<p><p>IntroductionMushrooms, belonging to the phyla Ascomycota and Basidiomycota, comprise approximately 14,000 known species, among which a small fraction are toxic. While toxic mushrooms are primarily associated with adverse health effects, recent research highlights their potential as sources of bioactive compounds with promising therapeutic applications.MethodsA systematic review was conducted using four major electronic databases: Web of Science, Google Scholar, PubMed, and ScienceDirect. The literature search, completed on July 1, 2024, utilized keywords including \"Poisonous mushrooms,\" \"Mushroom toxins,\" \"Mycotoxins,\" \"Beta-glucans,\" \"Psilocybin,\" and \"Therapeutic applications.\" Articles were selected based on specific inclusion criteria, focusing on studies investigating the biochemical, toxicological, and pharmacological properties of toxic mushroom compounds. Studies unrelated to mushrooms, non-peer-reviewed sources, or those with outdated or incomplete data were excluded.ResultsThis review examines key toxic mushroom compounds such as amanitins, phallotoxins, ibotenic acid, muscimol, orellanine, and gyromitrin, emphasizing their biosynthesis, structural features, and health effects. Despite their toxicity, compounds like beta-glucans, polysaccharides, lectins, and psilocybin exhibit immune-modulating, anticancer, and neuroprotective properties. These bioactive compounds have shown promise in targeting cancer stem cells and enhancing neurotransmitter activity, positioning them as potential therapeutic agents.DiscussionUnderstanding the therapeutic potential of toxic mushroom-derived bioactive compounds bridges toxicology and pharmacology, offering novel avenues for drug discovery. Comparative analysis with existing treatments highlights their unique advantages in modern medicine.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251323134"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of KIAA1429 on proliferation and invasion in oral cancer via LINC00958 methylation.","authors":"Pengjun Zhou, Wanning Li, Meiyi Ye, Chunlan Chen, Yifei Wang","doi":"10.1177/09603271251369056","DOIUrl":"10.1177/09603271251369056","url":null,"abstract":"<p><p>IntroductionThe investigation focused on the function of LINC00958 in the development of oral cancer, as well as the influence of methylation on tumor formation.MethodsTo explore the role of LINC00958, both its overexpression and its methylated form were examined in oral cancer cells. Various assays including CCK-8, transwell, plate cloning, flow cytometry, and EdU staining were utilized to assess the activity, invasion, cloning efficiency, cell cycle progression, and proliferation of the cancer cells. The tumorigenic potential of these cells was evaluated through experiments conducted on immunodeficient mice. Moreover, the methylation status of LINC00958 mediated by the KIAA1429 protein was confirmed using MeRIP-qPCR.ResultsThe study indicated that the overexpression of LINC00958 enhanced the activity, proliferation, and invasive capabilities of oral cancer cells, thereby increasing their tumorigenic potential. In contrast, overexpression of KIAA1429 led to a decrease in the proliferation, invasion, and tumorigenic properties of these cancer cells. Verification of methylation levels indicated that KIAA1429 overexpression resulted in heightened methylation of LINC00958. It was concluded that KIAA1429 diminishes the proliferation, invasion, and tumorigenesis of cancer cells through the methylation of LINC00958.DiscussionThis research provided insights into the role of LINC00958 in oral cancer cells and underscored the impact of methylation, offering a theoretical foundation for improving clinical diagnosis and treatment strategies for oral cancer patients.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251369056"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144823488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}