Biomolecules & biomedicine最新文献

{"title":"<i>TNFSF14 </i>and <i>CD44</i> are overexpressed in glioblastoma and associated with immunosuppressive microenvironment.","authors":"Alja Zottel, Neja Šamec, Ivana Jovčevska","doi":"10.17305/bb.2025.11791","DOIUrl":"10.17305/bb.2025.11791","url":null,"abstract":"<p><p>Glioblastoma (GBM) is one of the deadliest cancers, and the survival rate has remained low for decades. The aim of the study was the construction of the programmed death-ligand 1 (PD-L1) network, identification of its interactors and over-represented pathways, and analysis of the association between the identified genes and the immunosuppressive microenvironment of GBM. The PD-L1 network was constructed using Cytoscape and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING). Over-representation analysis was performed on WebGestalt using Kyoto Encyclopedia of Genes and Genomes (KEGG), Protein ANalysis THrough Evolutionary Relationships (Panther), and Reactome Pathway Database (Reactome). Gene expression levels were examined in silico using three large datasets (The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), and Rembrandt), as well as with qPCR. The association between PD-L1 gene expression and immune cell infiltration was analyzed using the Tumor Immune Estimation Resource (TIMER 2.0) online tool. Cluster of differentiation 44 (CD44) and tumor necrosis factor superfamily member 14 (TNFSF14) were found to be significantly overexpressed in GBM compared to lower-grade glioma (LGG) and normal brain tissue. Their overexpression was associated with worse overall survival and demonstrated a strong ability to differentiate between GBM and reference brain tissue. Notably, CD44 and TNFSF14 were linked to the mesenchymal subtype of GBM and positively correlated with the presence of regulatory T cells, resting natural killer (NK) cells, and PD-L1 expression. Our findings highlight the overexpression of CD44 and TNFSF14 in GBM and their potential involvement in creating an immunosuppressive microenvironment. Unraveling the PD-L1 interaction network and its associated pathways offers the potential not only to identify novel biomarkers for GBM prognosis but also to pinpoint alternative therapeutic targets that could be more effective in overcoming the immunosuppressive hurdles inherent in GBM treatment.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1829-1843"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging insights into mesenchymal stem cells and exosome-based therapies for liver injury.","authors":"Shaolong Yang, Juanyu Liu, Jia Siang Khe, Alvin Jiunn Hieng Lu, Vuanghao Lim","doi":"10.17305/bb.2025.12144","DOIUrl":"10.17305/bb.2025.12144","url":null,"abstract":"<p><p>Hepatic ischemia-reperfusion injury, fatty liver, liver fibrosis, liver peroxidative injury, and drug-induced liver injury are among the most common liver diseases. Mesenchymal stem cells (MSCs) possess multi-lineage differentiation potential and immunomodulatory functions. In the treatment of liver injury, MSCs can promote repair through homing effects, direct differentiation into hepatocyte-like cells (HLCs), immunomodulation, and anti-fibrotic mechanisms. Clinically, MSCs contribute to liver injury repair either directly or indirectly via the secretion of exosomes. Beyond their reparative role, MSC-derived exosomes can also serve as molecular biomarkers for the diagnosis and prognosis of liver diseases. Establishing higher-quality standards, robust auditing and evaluation systems, and conducting deeper mechanistic studies are essential prerequisites for the future clinical application of MSCs in the treatment of liver diseases.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1691-1708"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The molecular mechanisms of cuproptosis and its relevance to atherosclerosis.","authors":"Jiankang Wang, Zhian Chen, Hang Shang, Jiajuan Guo","doi":"10.17305/bb.2024.11826","DOIUrl":"10.17305/bb.2024.11826","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic inflammatory disease associated with lipid deposition in the vascular intima. Copper is a vital trace element implicated in the onset and progression of AS. Excessive intracellular copper accumulation induces a unique form of cell death termed \"cuproptosis.\" The emergence of the concept of cuproptosis has highlighted the potential role of copper in AS. This review explores the regulatory mechanisms of copper metabolism and cuproptosis, summarizes recent findings on the link between copper excess and AS, and examines how cuproptosis may influence AS progression. The goal is to propose novel diagnostic and therapeutic strategies for AS through the lens of cuproptosis.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1709-1722"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling.","authors":"Hui Li, Panpan Wang, Huijuan Chen, Yanyan Shao, Hui Luo","doi":"10.17305/bb.2025.11365","DOIUrl":"10.17305/bb.2025.11365","url":null,"abstract":"<p><p>Esophageal cancer (EC) is a highly aggressive malignancy with limited treatment options. Nei like DNA glycosylase 3 (NEIL3) and DNA topoisomerase II alpha (TOP2A) have been identified as potential therapeutic targets, though their roles in EC remain unclear. This study investigates the effects of NEIL3 overexpression and TOP2A knockdown, focusing on the WNT signaling pathway. ECA109 esophageal cancer cells were used to assess the impact of NEIL3 overexpression and TOP2A knockdown on proliferation, colony formation, migration, invasion, and apoptosis. The involvement of the WNT signaling pathway was also explored. NEIL3 overexpression significantly enhanced proliferation, colony formation, migration, and invasion while reducing apoptosis. In contrast, TOP2A knockdown suppressed these functions and promoted apoptosis, independent of NEIL3. NEIL3 overexpression could not reverse the effects of TOP2A knockdown. Both NEIL3 and TOP2A acted through the WNT signaling pathway. In vivo, NEIL3 knockdown reduced tumor size and weight via WNT pathway modulation. NEIL3 and TOP2A play key roles in EC progression through the WNT signaling pathway. Targeting these molecules may offer promising therapeutic strategies for EC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1844-1852"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morroniside ameliorates sevoflurane anesthesia-induced cognitive dysfunction in aged mice through modulating the TLR4/NF-κB pathway.","authors":"Jianxing Chen, Bo Peng, Wenqian Lin, Yinjun Mao, Yongsheng Wang","doi":"10.17305/bb.2024.11433","DOIUrl":"10.17305/bb.2024.11433","url":null,"abstract":"<p><p>Morroniside (Mor) is a bioactive compound in Cornus officinalis with anti-inflammatory, neuroprotective and antioxidant properties. Prolonged use of the anesthetic sevoflurane (Sev) has been connected to the development postoperative cognitive dysfunction (POCD). This research aims to elucidate the mechanism of action of Mor to improve cognitive impairment. A model of cognitive dysfunction induced by Sev was established in aged mice and tested for behavioral analysis using the water maze experiment. Histopathological changes and neuronal apoptosis in mouse hippocampus were observed by hematoxylin and eosin (HE) staining, Nissl staining, and TUNEL staining. ELISA and qRT-PCR determined the levels of inflammatory factors. Phenotypic transformation of microglia in hippocampal tissue was assessed by immunofluorescence, flow cytometry, and qRT-PCR. The interaction between Mor and TLR4 was analyzed using molecular docking. Western blot identified the levels of apoptosis-related proteins, synapse-related proteins, and TLR4/NF-κB pathway proteins. Inhalation of Sev caused a notable reduction in learning and spatial memory in old mice, which was dose-dependently ameliorated by Mor. Mor inhibited neuroinflammation, modulated the polarization state of hippocampal microglia, promoted their polarization to M2 type, alleviated Sev-induced hippocampal tissue damage and neuronal apoptosis. Notably, Mor can bind well with TLR4 and reduce TLR4-positive expression. Mor blocked Sev-induced TLR4/NF-κB pathway activation in hippocampal tissues, and the TLR4 agonist CRX-527 attenuated the effect of Mor. In conclusion, Mor blocked the TLR4/NF-κB pathway, reducing hippocampal tissue damage and neuroinflammation caused by Sev, which in turn improving cognitive impairment in aged mice.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1882-1894"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing CACYBP suppresses lung adenocarcinoma growth via CDK1 inhibition.","authors":"Ge Wen, Shaoqing Niu, Shiqi Mei, Senming Wang","doi":"10.17305/bb.2025.11849","DOIUrl":"10.17305/bb.2025.11849","url":null,"abstract":"<p><p>Calcyclin-binding protein (CACYBP) is a multidomain adaptor protein implicated in the development of various cancers. However, its molecular and biological roles in lung adenocarcinoma (LUAD) remain unclear. In this study, we aimed to elucidate the biological impact of CACYBP in LUAD. Immunohistochemistry was used to assess CACYBP expression in LUAD tissues. Lentivirus-mediated CACYBP knockdown was established in LUAD cell lines, and target gene expression was analyzed via Western blotting and qRT-PCR. Cell proliferation, apoptosis, and migration were evaluated using flow cytometry, colony formation assays, cell counting kit-8 (CCK 8) assays, Celigo cell counting, wound healing assays, Transwell assays, and mouse xenograft models. Co-immunoprecipitation was performed to verify the interaction between CACYBP and cyclin-dependent kinase 1 (CDK1). Additionally, the phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was used to investigate the involvement of CDK1 in the PI3K/AKT pathway. Our findings revealed that CACYBP was upregulated in LUAD tissues and correlated with advanced disease stages and poor prognosis. CACYBP knockdown inhibited LUAD progression and metastasis, promoted cell apoptosis in vitro, and reduced tumorigenicity in vivo. Mechanistically, we identified CDK1 as a direct interacting partner of CACYBP. CDK1 overexpression enhanced the malignant phenotype of LUAD cells and partially reversed the inhibitory effects of CACYBP knockdown. Furthermore, inhibition of the PI3K/AKT pathway using LY294002 significantly suppressed CDK1-mediated LUAD cell growth. In conclusion, CACYBP appears to function as a tumor promoter in LUAD, at least in part through CDK1-mediated activation of the PI3K/AKT pathway. These findings suggest that CACYBP could serve as a promising therapeutic target and a novel biomarker for LUAD prognosis.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1801-1815"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Andrographolide suppresses cervical cancer progression by targeting angiogenesis and inducing apoptosis in a CAM-PDX model.","authors":"Wanwan Zou, Jun Lou, Yun Yi, Yiming Cui, Xiaoyan Chu","doi":"10.17305/bb.2025.11432","DOIUrl":"10.17305/bb.2025.11432","url":null,"abstract":"<p><p>Cervical cancer poses significant clinical challenges, particularly in advanced stages. This study explores the therapeutic potential of andrographolide (AND), a bioactive compound derived from Andrographis paniculata, in mitigating cervical cancer progression using the chick embryo chorioallantoic membrane patient-derived xenograft (CAM-PDX) model. The model was validated through hematoxylin-eosin (H&E) staining and immunohistochemistry, which confirmed its ability to accurately replicate the histological and molecular characteristics of patient-derived xenografts (PDXs), establishing its reliability for therapeutic screening. A dose of 20 mg/kg AND was selected for further evaluation based on preliminary chorioallantoic membrane (CAM) assay findings. In the CAM-PDX model, AND significantly inhibited tumor growth, primarily by reducing angiogenesis and vessel density. Immunohistochemical analysis revealed that AND downregulated key proteins associated with cancer cell proliferation and survival, including Ki67, B-cell lymphoma 2 (BCL-2), and Erythroblast transformation-specific-related gene (ERG). These results indicate that AND not only disrupts tumor angiogenesis but also induces cell cycle arrest and promotes apoptosis in cervical cancer cells. In summary, this study successfully established a reproducible CAM-PDX model for drug evaluation and highlighted the potential of AND as a promising therapeutic candidate for cervical cancer, warranting further clinical investigation.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1780-1788"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Fascin-1 in cervical cancer metastasis via Wnt/β-catenin pathway activation.","authors":"Yan Wang, Wei Cui, Dong-Mei Chu","doi":"10.17305/bb.2025.12114","DOIUrl":"10.17305/bb.2025.12114","url":null,"abstract":"<p><p>This investigation delves into the impact of Fascin-1, a protein known for its role in actin bundling and its association with metastatic enhancement, on the advancement of cervical cancer (CC). Elevated levels of Fascin-1 have been observed in metastatic carcinomas, but its impact on gene regulation in CC has not been thoroughly studied. Our research demonstrates a marked elevation in the expression of Fascin-1 within tissues affected by CC. Experiments employing both overexpression and knockdown methods revealed that Fascin-1 plays a critical role in promoting the proliferation and mobility of CC cells in vitro. Correspondingly, reducing Fascin-1 levels led to a marked decrease in tumor growth and metastatic spread in vivo. At the molecular level, diminishing Fascin-1 expression resulted in decreased β-catenin and C-myc RNA and protein levels. This implies that Fascin-1 could intensify the progression of CC by influencing the Wnt/β-catenin signaling cascade. This study not only elucidates the mechanism by which Fascin-1 contributes to the advancement of CC but also proposes a novel approach for therapeutic intervention.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1789-1800"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Synthesis, characterization, and <i>in vitro</i>-<i>in ovo</i> toxicological screening of silibinin fatty acids conjugates as prodrugs with potential biomedical applications.","authors":"Cristina Dehelean, Simona Cinta Pinzaru, Adrian Pirnau, Vasile Chis, Andrea Simion, Geza Lazar, Andrada Iftode, Iasmina Marcovici, Ersilia Alexa, Estera Boeriu","doi":"10.17305/bb.2025.12570","DOIUrl":"10.17305/bb.2025.12570","url":null,"abstract":"<p><p>Corrected article:  https://www.bjbms.org/ojs/index.php/bjbms/article/view/10600 The affiliation of the first author, Cristina Adriana Dehelean, was incomplete in the originally published version of this article. One of the authors asked to add her third institutional affiliation. The correct affiliations for Cristina Adriana Dehelean are as follows: 1Faculty of Pharmacy, \"Victor Babeș\" University of Medicine and Pharmacy Timișoara, Timișoara, Romania 2Research Center for Pharmaco-Toxicological Evaluations, Faculty of Pharmacy, \"Victor Babeș\" University of Medicine and Pharmacy Timișoara, Timișoara, Romania 3Faculty of Food Engineering, University of Life Sciences \"King Michael I\" from Timișoara, Timișoara, Romania. We apologize to the readership for any inconvenience caused.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1896"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>TBRG4</i> as a prognostic biomarker and key regulator of cell cycle and EMT in lung cancer.","authors":"Ansheng Wang, Qiao Ge, Zhenkai Fan, Bing Xia, Zhao Jin, Haitao Liu, Haiwei Sang, Qicai Li, Congli Zhang, Haonan Zhu","doi":"10.17305/bb.2025.11353","DOIUrl":"10.17305/bb.2025.11353","url":null,"abstract":"<p><p>Transforming growth factor β regulator 4 (TBRG4) is upregulated in lung cancer, but its biological role and underlying mechanisms remain poorly understood. In this study, we analyzed pancancer gene expression profiles and clinical data from University of California, Santa Cruz Xena (UCSC Xena) to evaluate the prognostic significance of TBRG4 using univariate and multivariate Cox regression analyses. Genes with a Pearson correlation coefficient above 0.4 with TBRG4 in lung cancer were identified via UALCAN, followed by pathway enrichment analyses to explore their functional associations. To investigate TBRG4's role in lung cancer progression, we assessed cell proliferation, colony formation, and cell cycle alterations in lung cancer cells following TBRG4 knockdown. Western blot analysis was performed to examine the effects of TBRG4 depletion on key cell cycle regulators and epithelial-mesenchymal transition (EMT) markers. Additionally, the biological significance of TBRG4 was evaluated in vivo using a mouse xenograft model. TBRG4 knockdown significantly inhibited cell proliferation and colony formation while inducing cell cycle arrest and apoptosis in lung cancer cells. Analysis of co-expressed genes in the The Cancer Genome Atlas - Lung Adenocarcinoma (TCGA-LUAD) cohort revealed enrichment in cell cycle-related pathways, aligning with our experimental findings. Furthermore, TBRG4 depletion reduced EMT marker expression and suppressed tumor growth in vivo. Collectively, these findings suggest that TBRG4 may serve as a promising prognostic biomarker and therapeutic target in lung cancer.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1816-1828"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}