{"title":"EGR3转录上调肝癌DCN表达抑制肿瘤进展","authors":"Hong Yang, Da Sun, Bin Zhang, Chun Yu","doi":"10.1002/jbt.70399","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Decorin (DCN), a multifunctional extracellular matrix protein, has been reported to exhibit tumor-suppressive effects in various cancers, including liver cancer. However, the transcriptional regulatory mechanisms of DCN in liver cancer remains unclear. We analyzed DCN expression in liver cancer cells using qPCR and Western blot. Functional assays (CCK-8, colony formation, flow cytometry, and Transwell) were performed to assess the effects of DCN overexpression (via pcDNA3.1-DCN) on proliferation, apoptosis, invasion, and migration. Bioinformatics tools (PROMO and UCSC) predicted EGR3 as a potential transcriptional regulator of DCN, which was validated through ChIP and luciferase reporter assays. Rescue experiments (si-EGR3+pcDNA3.1-DCN cotransfection) were conducted to confirm the DCN-EGR3 regulatory axis. DCN was significantly downregulated in liver cancer cells. Its overexpression suppressed proliferation, invasion, and migration while promoting apoptosis. Mechanistically, EGR3 was identified as a transcriptional activator of DCN, and EGR3 knockdown reversed the tumor-suppressive effects of DCN. Our findings demonstrated that DCN exerted antitumor effects in liver cancer via transcriptional activation by EGR3, providing a novel therapeutic target for liver cancer treatment.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 7","pages":""},"PeriodicalIF":3.2000,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"EGR3 Transcriptionally Upregulates the Expression of DCN in Liver Cancer to Inhibit Tumor Progression\",\"authors\":\"Hong Yang, Da Sun, Bin Zhang, Chun Yu\",\"doi\":\"10.1002/jbt.70399\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>Decorin (DCN), a multifunctional extracellular matrix protein, has been reported to exhibit tumor-suppressive effects in various cancers, including liver cancer. However, the transcriptional regulatory mechanisms of DCN in liver cancer remains unclear. We analyzed DCN expression in liver cancer cells using qPCR and Western blot. Functional assays (CCK-8, colony formation, flow cytometry, and Transwell) were performed to assess the effects of DCN overexpression (via pcDNA3.1-DCN) on proliferation, apoptosis, invasion, and migration. Bioinformatics tools (PROMO and UCSC) predicted EGR3 as a potential transcriptional regulator of DCN, which was validated through ChIP and luciferase reporter assays. Rescue experiments (si-EGR3+pcDNA3.1-DCN cotransfection) were conducted to confirm the DCN-EGR3 regulatory axis. DCN was significantly downregulated in liver cancer cells. Its overexpression suppressed proliferation, invasion, and migration while promoting apoptosis. Mechanistically, EGR3 was identified as a transcriptional activator of DCN, and EGR3 knockdown reversed the tumor-suppressive effects of DCN. Our findings demonstrated that DCN exerted antitumor effects in liver cancer via transcriptional activation by EGR3, providing a novel therapeutic target for liver cancer treatment.</p></div>\",\"PeriodicalId\":15151,\"journal\":{\"name\":\"Journal of Biochemical and Molecular Toxicology\",\"volume\":\"39 7\",\"pages\":\"\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-07-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biochemical and Molecular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70399\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biochemical and Molecular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70399","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
EGR3 Transcriptionally Upregulates the Expression of DCN in Liver Cancer to Inhibit Tumor Progression
Decorin (DCN), a multifunctional extracellular matrix protein, has been reported to exhibit tumor-suppressive effects in various cancers, including liver cancer. However, the transcriptional regulatory mechanisms of DCN in liver cancer remains unclear. We analyzed DCN expression in liver cancer cells using qPCR and Western blot. Functional assays (CCK-8, colony formation, flow cytometry, and Transwell) were performed to assess the effects of DCN overexpression (via pcDNA3.1-DCN) on proliferation, apoptosis, invasion, and migration. Bioinformatics tools (PROMO and UCSC) predicted EGR3 as a potential transcriptional regulator of DCN, which was validated through ChIP and luciferase reporter assays. Rescue experiments (si-EGR3+pcDNA3.1-DCN cotransfection) were conducted to confirm the DCN-EGR3 regulatory axis. DCN was significantly downregulated in liver cancer cells. Its overexpression suppressed proliferation, invasion, and migration while promoting apoptosis. Mechanistically, EGR3 was identified as a transcriptional activator of DCN, and EGR3 knockdown reversed the tumor-suppressive effects of DCN. Our findings demonstrated that DCN exerted antitumor effects in liver cancer via transcriptional activation by EGR3, providing a novel therapeutic target for liver cancer treatment.
期刊介绍：
The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
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