Molecular Biology Reports最新文献

{"title":"Regulation of vascular smooth muscle cells phenotype by metformin up-regulated miR-1/ CCND1 axis via targeting AMPK/TGF-β signaling pathway.","authors":"Yulin Luo, Mengting Li, Jingcan You, Jun Jiang, Min Zeng, Mao Luo","doi":"10.1007/s11033-025-10532-0","DOIUrl":"https://doi.org/10.1007/s11033-025-10532-0","url":null,"abstract":"<p><p>The phenotypic switch of vascular smooth muscle cells (VSMCs), characterized by the tissue-specific expression of certain microRNAs (miRNAs), is a critical factor in the development of diabetic vascular diseases. Metformin, a widely prescribed anti-diabetic medication for type 2 diabetes treatment, activates the adenosine monophosphate-activated protein kinase (AMPK) pathway and exerts a protective effect on vascular endothelium. Although the regulatory effects of metformin on the switch of the vascular smooth muscle cell phenotype have been identified, the specific role of miRNAs in this process remains unclear. We identified a specific miR-1 in response to metformin treatment and determined its effects on both miR-1 and its targets. Subsequently, we investigated the influence of these factors on the metformin-induced phenotype switch in vascular smooth muscle cells, specifically focusing on proliferation and migration, as well as activation of the AMPK/Transforming Growth Factor (TGF-β) axis. This was achieved using various methodologies, including bioinformatics analysis, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis, wound scratch assays, and Cell Counting Kit-8 assays. Our findings showed that metformin upregulated miR-1, which directly targets cyclin D1 (CCND1) in VSMCs. Metformin was observed to enhance the expression of contractile phenotype proteins, including α-smooth muscle actin (α-SMA) and smooth muscle myosin heavy chain (SMMHC), while simultaneously reducing the expression of proliferative phenotype proteins such as CCND1 and proliferating cell nuclear antigen (PCNA). The inhibition of miR-1 was found to reverse the effects of metformin on the phenotypic switch of VSMCs. This occurs partly through the AMPK/TGF-β signaling pathway and inhibits the migration and proliferation of VSMCs.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"437"},"PeriodicalIF":2.6,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010072","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}

{"title":"Role of traditional and new biomarkers in the assessment of chronic kidney diseases: a comprehensive analysis of the biochemical, molecular and clinical dimensions.","authors":"Arumugam Suresh, Natarajan Muninathan, Shobana Sampath, Sandhanasamy Devanesan, Mohamad S AlSalhi, D Manoj","doi":"10.1007/s11033-025-10498-z","DOIUrl":"https://doi.org/10.1007/s11033-025-10498-z","url":null,"abstract":"<p><strong>Background: </strong>Kidney function is necessary for the diagnosis and treatment of renal diseases. Traditional biomarkers like creatinine have limitations due to their susceptibility to interference and fluctuation. This study's objective is to test and compare the efficacy of conventional and innovative biomarkers in evaluating kidney function and disease.</p><p><strong>Methods: </strong>We looked at creatinine, cystatin C, parathyroid hormone (PTH), electrolytes, interleukin-6 (IL-6), C-reactive protein (CRP), the APA I gene, and kidney injury molecule-1 (KIM-1). The present study focused on the stability, sensitivity, and specificity of biomarkers using a combination of traditional and innovative analytical techniques.</p><p><strong>Results: </strong>Present results showed that creatinine, although commonly used as a measure, frequently overestimates renal function as a result of chromogenic interference. On the other hand, cystatin C showed better sensitivity and was less reliant on influences outside the kidneys. Kidney biomarkers, such as KIM-1, exhibit the potential for identifying acute kidney injury at an early stage. Furthermore, there was a positive correlation between increased levels of CRP and PTH and the progression of kidney disease to more advanced stages.</p><p><strong>Conclusion: </strong>This study emphasizes the importance of combining traditional and new biomarkers to improve the accuracy of diagnosing and managing kidney illness. The more effective use of biomarkers will result in improved patient outcomes.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"434"},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144064292","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}

{"title":"Trans-anethole enhances mesenchymal stem cell derived exosomes function to inhibit H₂O₂-induced rheumatoid arthritis-like inflammation in HIG-82 synovial cells.","authors":"Tai-Lung Huang, Yu-Chun Chang, Wei-Wen Kuo, Shih-Wen Kao, Chia-Hua Kuo, Dennis Jine-Yuan Hsieh, Kuan-Ho Lin, Tsung-Jung Ho, Chih-Yang Huang","doi":"10.1007/s11033-025-10426-1","DOIUrl":"https://doi.org/10.1007/s11033-025-10426-1","url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) is an auto-immune inflammatory disorder for which an effective cure is yet to be found. Trans-anethole (1-methoxy-4-(1E)-1-propen-1-yl-benzene), a key bioactive compound derived from the perennial plant Foeniculum vulgare, exerts multiple medicinal benefits. In this study, we investigated the therapeutic potential of exosomes derived from anethole-preconditioned human Wharton Jelly-derived mesenchymal stem cells (hWJMSCs) against RA-like inflammation in H₂O₂-treated synoviocyte HIG-82 cells.</p><p><strong>Methods: </strong>The fennel samples were prepared and trans-anethole was purified using LC-ESI-MS/MS analysis. The MTT cell viability assays, hWJMSC derived exosomes, and expression analysis of cellular markers related to proliferation, stemness, apoptosis, and extracellular matrix (ECM)-degrading proteases were performed using Western blotting in HIG-82 cells.</p><p><strong>Results: </strong>The results showed that anethole treatment significantly increased cell viability and expression of the MSC marker CD90 in a dose-dependent manner in HIG-82 cells. Cell stemness markers, including proliferation markers cyclin-D, proliferating cell nuclear antigen (PCNA), and minichromosome maintenance complex component 2 (MCM2) were enhanced, whereas p53 and p21 were decreased by anethole. Exosomes derived from anethole-preconditioned hWJMSCs significantly improved the cell viability of H₂O₂-treated HIG-82 cells. Anethole- preconditioned exosomes decreased ECM-degrading proteases MMP-13, ADAMTS-2, -8, and -17, and AQP-3 expression more significantly than exosomes without preconditioned hWJMSC. Bcl-2 was increased, whereas Bax, Cyto c, and c-caspase 3 were decreased by preconditioned exosomes more prominently than exosomes from without preconditioned hWJMSCs in H₂O₂-treated HIG-82 cells.</p><p><strong>Conclusion: </strong>Together, the study showed that exosomes derived from anethole-preconditioned hWJMSC have a greater potential to inhibit RA-like inflammation and apoptosis in H₂O₂-treated HIG-82 cells.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"431"},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028012","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}

{"title":"The link between the trans-Golgi network and tumour progression.","authors":"Leila Jahangiri","doi":"10.1007/s11033-025-10548-6","DOIUrl":"https://doi.org/10.1007/s11033-025-10548-6","url":null,"abstract":"<p><p>The trans-Golgi network is a major sorting organelle consisting of a tubular membrane originating from the trans-Golgi cisternae. Proteins and lipids synthesised in the endoplasmic reticulum are transported through the Golgi apparatus and sorted in the trans-Golgi network into pleomorphic transport carriers targeted for various destinations. These destinations include the apical and basolateral membranes, early and late, recycling endosomes, and secretory granules. The trans-Golgi network also accepts retrograde endosome traffic, contributing to the recycling of proteins and lipids, and, therefore, sits at the crossroads of secretory and endosomal systems. Cancer is a somatic evolutionary process that comprises the accumulation of mutations that contribute to tumourigenesis, growth, progression, immune evasion, and resistance to therapy. This study aims to catalogue how multiple components and players of the trans-Golgi network affect tumour progression. Further, the link between the tumour microenvironment, the trans-Golgi network, and tumour progression will be dissected. A more profound understanding of these mechanisms will inform better treatment options.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"435"},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144027897","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":"Antimicrobial peptides: evolving soldiers in the battle against drug-resistant superbugs.","authors":"Piyush Baindara, Sumeeta Kumari, Roy Dinata, Santi M Mandal","doi":"10.1007/s11033-025-10533-z","DOIUrl":"https://doi.org/10.1007/s11033-025-10533-z","url":null,"abstract":"<p><p>The discovery of antibiotics was one of the greatest achievements in human history, however, antibiotic resistance evolved no later than the introduction of antibiotics. The rapid evolution of antibiotic-resistant pathogens soon became frightening and remained a global healthcare threat. There is an urgent need to have new alternatives or new strategies to combat the multi-drug resistant superbugs such as methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), carbapenem-resistant Pseudomonas aeruginosa (CR-PA), extended-spectrum β-lactamases (ESBL) bearing multidrug-resistant Acinetobacter baumannii (MDR-AB), Escherichia coli (E. coli), and Klebsiella pneumoniae (K. pneumoniae). Antimicrobial peptides (AMPs) have been considered promising agents equipped with unique mechanisms of action along with several other benefits to fight the battle against drug-resistant superbugs. Overall, the current review summarizes the mechanisms of drug-resistant development, the mechanism of action adopted by AMPs to combat drug-resistant pathogens, and the immunomodulatory properties of AMPs. Additionally, we have also reviewed the synergistic potential of AMPs with conventional antibiotics along with the associated challenges and limitations of AMPs in the way of pharmacological development for therapeutic applications in clinical settings.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"432"},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971665","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}

{"title":"LncRNA MEG3 independently collaborates with lncRNA TUG1 to prevent cholesterol efflux in ox-LDL-induced human umbilical vein endothelial cells.","authors":"Yong Jiang, Ying Zhao, Bo-Yan Jia, Sheng-Yu Zhong, Jian-Feng Cheng, Zi-Qi Yu","doi":"10.1007/s11033-025-10516-0","DOIUrl":"https://doi.org/10.1007/s11033-025-10516-0","url":null,"abstract":"<p><strong>Background: </strong>Maternally expressed gene 3 (MEG3) is an abnormal methylation gene and low expression of lncRNA MEG3 have been observed in coronary heart disease (CHD). This study aims to investigate whether DNA methylation mediates the abnormal expression of lncRNA MEG3 and to explore the underlying mechanism by which lncRNA MEG3 regulates cholesterol efflux.</p><p><strong>Methods: </strong>Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to assess molecular expressions. Oxidized low-density lipoprotein (Ox-LDL) treated human umbilical vein endothelial cells (HUVECs) were established as an in vitro model. Methylation-specific PCR was used to evaluate the methylation level of MEG3. BODIPY-cholesterol assay was performed to examine intracellular cholesterol efflux. Luciferase reporter gene assay was used to verify the interaction between miR-181a-5p and MEG3/ABCA1.</p><p><strong>Results: </strong>LncRNA MEG3 was downregulated, while taurine upregulated gene 1 (TUG1) was upregulated in patients with CHD. Besides, ox-LDL treatment increased DNMT3B expression, decreased lncRNA MEG3 expression and elevated the level of MEG3 methylation in HUVECs. Further experiments showed that DNMT3B overexpression reduced lncRNA MEG3 expression and enhanced MEG3 methylation. Additionally, silencing MEG3 decreased ABCA1 expression to prevent cholesterol efflux in HUVECs. The interaction between miR-181a-5p and MEG3/ABCA1 were also confirmed. Rescue experiments suggested that MEG3 knockdown downregulated ABCA1 expression via miR-181a-5p, thereby preventing cholesterol efflux in HUVECs. Furthermore, the results showed that MEG3 collaborated with TUG1 in an independent manner to block ABCA1 mediated-cholesterol efflux in HUVECs.</p><p><strong>Conclusion: </strong>Downregulation of lncRNA MEG3, mediated by DNMT3B, prevents cholesterol efflux through miR-181a-5p/ABCA1 axis in ox-LDL-induced HUVECs. Moreover, MEG3 collaborated with TUG1 in an independent manner to prevent ABCA1 mediated-cholesterol efflux in HUVECs.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"433"},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008068","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}

{"title":"Chrysin improves endothelial inflammation via the NFAT pathway in Kawasaki disease.","authors":"Jin Ma, Yan Li, Yunjia Tang, Guanghui Qian, Haitao Lv, Xiudao Song, Ying Liu","doi":"10.1007/s11033-025-10529-9","DOIUrl":"https://doi.org/10.1007/s11033-025-10529-9","url":null,"abstract":"<p><strong>Background: </strong>The purpose of this study was to evaluate the therapeutic effects of Chrysin on endothelial inflammation in a KD mouse model and to elucidate the molecular mechanisms underlying these effects, with a particular focus on the NFAT2 signaling pathway.</p><p><strong>Methods and results: </strong>In vivo, a KD mouse model was used to assess the effects of Chrysin on coronary artery inflammation. Histological analysis, immunohistochemistry, and cytokine profiling were performed to evaluate inflammatory cell infiltration, structural changes in the arteries, and modulation of key inflammatory cytokines. In vitro, TNFα-stimulated HCAECs were used to examine the protective effects of Chrysin on endothelial injury, including cytokine secretion and adhesion molecule expression. Mechanistic studies were conducted to explore the role of the NFAT2 signaling pathway in mediating Chrysin's effects, utilizing molecular docking analysis and Western blotting. In vivo, Chrysin treatment significantly alleviated coronary artery inflammation in the KD mouse model. Histological analysis revealed reduced inflammatory cell infiltration and improved elastin fiber structure. Cytokine analysis showed that Chrysin attenuated the elevated levels of IL-6, IL-17, TNFα, and MCP-1 in KD mice. In vitro, Chrysin reduced TNFα-induced endothelial injury, as evidenced by decreased secretion of IL-6, IL-8, IL-23, ICAM-1 and VCAM-1 in HCAECs. Mechanistic investigations revealed that Chrysin's effects on endothelial inflammation were mediated through the NFAT2 signaling pathway, rather than the upstream PLCγ1 pathway, as confirmed by molecular docking and Western blotting. Inhibition of PLCγ1 did not alter the protective effects of Chrysin, suggesting that its action is primarily through NFAT2.</p><p><strong>Conclusions: </strong>This study provides the first evidence that Chrysin significantly reduces endothelial inflammation and vascular injury in KD. The observed anti-inflammatory effects are mediated through the NFAT2 signaling pathway, highlighting the potential of Chrysin as a therapeutic agent for managing KD and its associated vascular complications.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"428"},"PeriodicalIF":2.6,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033788","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}

{"title":"The role of the casein kinase 1 (CK1) family in fungal infections.","authors":"Meiling Wu, Haolin Zhang, Miao Jia, Xingyu Cao, Juan Wang","doi":"10.1007/s11033-025-10526-y","DOIUrl":"https://doi.org/10.1007/s11033-025-10526-y","url":null,"abstract":"<p><p>The Casein kinase 1 (CK1) family, as an important member of the protein kinase family, exhibits high evolutionary conservation and is widely distributed in various cell types. CK1 plays critical roles in numerous cellular biological processes, and its abnormal expression is closely associated with the development and progression of various diseases. The CK1 protein family has been extensively studied and reported as an influential factor in various mammalian diseases. Increasing evidence indicates that the CK1 family also plays an indispensable role in fungal growth and infection processes. For example, CK1 protein in Candida albicans plays a crucial role in virulence and drug resistance; CK1 protein in Cryptococcus neoformans affects cell integrity and stress response; and CK1 protein in Magnaporthe oryzae and Fusarium graminearum is involved in fungal growth, conidiation, and pathogenesis. Advances in protein kinase inhibitor research, particularly through enhanced understanding of kinase-substrate interactions and species-specific structural features, are poised to enable the development of highly specific fungal CK1 inhibitors with improved anti-fungi indices.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"430"},"PeriodicalIF":2.6,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032735","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}

{"title":"Unlocking the potential of Bavachin in vitamin D receptor cascade modulation for rheumatoid arthritis.","authors":"Debolina Chakraborty, Lovely Joshi, Prachi Agnihotri, Swati Malik, Niyati Pal, Vijay Kumar, Sagarika Biswas","doi":"10.1007/s11033-025-10530-2","DOIUrl":"https://doi.org/10.1007/s11033-025-10530-2","url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by joint damage and disrupted vitamin D signaling, leading to calcium deposition in joints. This study explores the therapeutic potential of Bavachin (BVN), a phytoestrogen from Psoralea corylifolia, in modulating vitamin D signaling in RA.</p><p><strong>Methods: </strong>Vitamin D receptor (VDR) structure was modeled using SWISS-MODEL, AlphaFold, and I-TASSER, followed by docking with BVN and Estradiol (E2) via AutoDock Vina. BVN's effects on VDR mRNA and protein levels in RA-FLS were assessed by qRT-PCR and Western blot(WB). VDR-related BVN targets in RA were explored through protein-protein interaction (PPI) network and pathway analysis in Cytoscape. BVN's impact on RXRα expression and VDR-RXRα interaction was examined by WB and immunofluorescence. Alizarin staining evaluated calcium deposition, while qRT-PCR analyzed BVN's regulation of calcium-binding proteins.</p><p><strong>Results: </strong>In silico analysis revealed a strong interaction of VDR with BVN with Gibbs-free energy of -7.2 Kcal/mol with prominent H-bonds. Further, in vitro study in RA-FLS revealed that BVN treatment increased VDR mRNA and protein expression. PPI and pathway enrichment analysis retrieved RXRα as the prominent protein to be targeted by BVN in Vitamin D signaling. BVN treatment also significantly upregulated RXRα expression and enhanced the interaction between VDR and RXRα. Further, BVN modulated associated calcium signaling, reduced calcium deposition in RA-FLS and significantly downregulated calcium-binding proteins CALB1, CALB2, NCX1, TRPV5, and TRPV6.</p><p><strong>Conclusion: </strong>Collectively, this study depicted a prominent therapeutic efficacy of BVN in targeting Vitamin D signaling and associated calcium deposition to alleviate RA pathogenesis.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"429"},"PeriodicalIF":2.6,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035535","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}

{"title":"CHD1 dysregulation in cancer: bridging chromatin instability, therapy resistance, and immune evasion.","authors":"K S Praveen Kumar, M N Jyothi, Akila Prashant","doi":"10.1007/s11033-025-10536-w","DOIUrl":"https://doi.org/10.1007/s11033-025-10536-w","url":null,"abstract":"<p><p>Chromodomain-Helicase-DNA-binding protein 1 (CHD1) is a central regulator of chromatin dynamics, profoundly influencing gene expression, DNA repair, and genomic stability. This review critically explores CHD1's role in cancer biology, emphasizing its complex, context-dependent functions. In prostate cancer, CHD1 acts as both a tumour suppressor and a facilitator of neuroendocrine differentiation, with its loss linked to aggressive phenotypes, resistance to androgen receptor therapies, and synthetic lethality with PTEN loss. Beyond prostate cancer, CHD1 is implicated in breast, ovarian, and hematological cancers, where it modulates chromatin accessibility, transcription regulation, and therapy resistance. Despite its promise as a biomarker and therapeutic target, CHD1 presents challenges due to its dual roles and cancer-specific effects. The review also highlights critical gaps, including the need for high-resolution studies on CHD1's interactions with immune pathways, synthetic lethality mechanisms, and chromatin remodelling in treatment resistance. Leveraging CHD1's molecular complexities could show the way for innovative diagnostic and therapeutic strategies in cancer, but its role in non-prostate cancers remains underexplored, warranting further investigation.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"426"},"PeriodicalIF":2.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002007","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}