Biochemistry and Biophysics Reports最新文献

{"title":"Nardilysin regulates <i>Slc2a2</i> expression via an ISLET1-dependent enhancer mechanism in pancreatic β-cells.","authors":"Kiyoto Nishi, Narangerel Ganbaatar, Mikiko Ohno, Shinya Ikeda, Hirotaka Iwasaki, Mend Amar Batbaatar, Enkhjin Gansukh, Eiichiro Nishi","doi":"10.1016/j.bbrep.2026.102772","DOIUrl":"10.1016/j.bbrep.2026.102772","url":null,"abstract":"<p><p>GLUT2 (<i>Slc2a2</i>) is a key glucose transporter in pancreatic β-cells, and its reduced expression is closely linked to defective glucose-stimulated insulin secretion (GSIS) and diabetes. We previously reported that pancreatic β-cell-specific nardilysin (NRDC)-deficient mice (BetaKO) exhibit a severe diabetic phenotype with defective GSIS and reduced <i>Slc2a2</i> expression in islets. However, because BetaKO mice also showed reduced MafA, a key upstream regulator of <i>Slc2a2</i>, along with an increased α-cell/β-cell ratio and other secondary changes that could influence GLUT2 levels, the mechanism by which NRDC regulates <i>Slc2a2</i> transcription remained unclear. Here, we demonstrate that NRDC controls <i>Slc2a2</i> expression in a β-cell-autonomous and MafA-independent manner. By integrating publicly available ATAC-seq and ChIP-seq datasets, we identified four active enhancer regions around the murine <i>Slc2a2</i> locus, two of which are evolutionarily conserved in human islets. Luciferase assays in MIN6 β-cells revealed that NRDC selectively controls the activity of a conserved enhancer located 39 kb downstream of the <i>Slc2a2</i> transcription start site. Chromatin immunoprecipitation (ChIP) and re-ChIP assays further revealed that, in MIN6 cells, NRDC occupies this enhancer and is required for efficient recruitment of ISLET1, a transcription factor upstream of <i>Slc2a2</i>. These findings suggest that NRDC contributes to <i>Slc2a2</i> regulation in addition to MafA, highlighting multifaceted roles of NRDC in pancreatic β-cell gene regulation.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"102772"},"PeriodicalIF":3.3,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13571273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963025","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":"Nuclear localisation of a fish-derived ice-binding protein and related transcriptional changes in <i>Caenorhabditis elegans</i>.","authors":"Saki Nakamura, Kazuki Ozawa, Kotaro Ozaki, Yoichi Shinkai, Masahiro Kuramochi","doi":"10.1016/j.bbrep.2026.102771","DOIUrl":"10.1016/j.bbrep.2026.102771","url":null,"abstract":"<p><p>Ice-binding proteins (IBPs) are functional molecules that enable organisms to survive severe cold by binding specifically to ice crystals and suppressing their growth and recrystallisation. Although their primary role has traditionally been viewed as antifreeze activity, recent studies have suggested additional cell-protective functions, including possible effects on membrane stability. Heterologous expression of the fish type III IBP NfeIBP in <i>Caenorhabditis elegans</i> has previously been shown to increase tolerance to cold and freezing stress. However, the understanding of the intracellular localisation of IBPs in vivo and their effects on gene expression remains limited. Here, we examined the intracellular localisation and associated cellular effects of the fish-derived IBP variant NfeIBP6(A20I), which is known to confer strong cold tolerance in <i>C. elegans</i>. An NfeIBP6(A20I)-wrmScarlet fusion protein expressed in body wall muscle cells was detected in both cytoplasmic and nuclear regions and partially overlapped with the nuclear marker NLSsfGFP, indicating its presence within nuclear compartment. Expression of NfeIBP6(A20I) did not cause detectable abnormalities in the physiological traits examined. Transcriptomic analysis further revealed biased changes in gene expression, with substantially more downregulated genes than upregulated genes. The downregulated genes were significantly enriched in biological processes related to cuticle development and immune response. These findings indicate that NfeIBP6(A20I) exhibits previously unrecognised intracellular behaviour in <i>C. elegans</i> and suggest that the functional scope of IBPs may extend beyond their conventional role in ice binding.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"102771"},"PeriodicalIF":3.3,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13571282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963066","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":"Reduction of cell viability and alteration of genomic DNA methylation by phthalates in a normal human fibroblast (NHF) cell line in vitro","authors":"Warqaa Y. Salih,&nbsp;Fikrat M. Hassan,&nbsp;Majeed A. Sabbah","doi":"10.1016/j.bbrep.2026.102755","DOIUrl":"10.1016/j.bbrep.2026.102755","url":null,"abstract":"<div><div>Phthalates are ubiquitous environmental contaminants widely used as plasticizers in poly vinyl chloride products, and growing evidence implicates them in metabolic activity reduction and epigenetic dysregulation. However, their direct effects on non-transformed human cells remain incompletely characterized. The present <em>in vitro</em> study evaluated the reduction in cell viability and DNA methylation–modulating effects of three widely distributed phthalates, di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DnBP), and di-isononyl phthalate (DINP), on normal human fibroblast (NHF) cells. Cells were exposed to serial concentrations (31.25–1000 μg/mL) for 72 h, and the viability was assessed by MTT assay, followed by IC₅₀ determination via nonlinear regression. Global DNA methylation was subsequently quantified at the IC₅₀ concentration by ELISA-based measurement of 5-methylcytosine (5-mC). All three phthalates produced significant concentration-dependent reductions in cell viability. Constraining the regression plateaus to 100% and 0% viability yielded estimated IC₅₀ values of 19.2 μg/mL for DEHP, 43.4 μg/mL for DnBP, and 13.1 μg/mL for DINP; as viability fell below 50% at the lowest concentration tested, these values represent extrapolation below the sampled range, their confidence intervals overlap, and no potency ranking is asserted. At fixed high-effect concentrations, DEHP and DINP significantly elevated global 5-mC levels to 189.18% and 159.56% of control, respectively, whereas DnBP induced only a non-significant increase (120.06%). These findings indicate that phthalates compromise both the viability and epigenetic integrity of NHF cells in a congener-specific manner, underscoring their potential contribution to methylation-associated human pathologies.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102755"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13506537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148824728","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":"Mechanism of FXR signaling: from liver inflammation to hepatocellular carcinoma","authors":"Cheng Qiuluo,&nbsp;Huang Guiqun,&nbsp;Han Xue,&nbsp;Zhu Ying","doi":"10.1016/j.bbrep.2026.102753","DOIUrl":"10.1016/j.bbrep.2026.102753","url":null,"abstract":"<div><h3>Objective</h3><div>To clarify the core regulatory role and molecular mechanism of farnesoid X receptor (FXR) in the progression from liver inflammation/fibrosis to hepatocellular carcinoma (HCC), and to provide a theoretical basis for targeted prevention and treatment of liver diseases.</div></div><div><h3>Methods</h3><div>A systematic review was performed to integrate FXR's key regulatory mechanisms in bile acid homeostasis, inflammatory signaling, metabolic reprogramming, tumor pathways, and the tumor immune microenvironment. Intervention effects of natural compounds and FXR agonists/antagonists were analyzed for clinical translational potential.</div></div><div><h3>Results</h3><div>FXR acts as a core regulator throughout the inflammation–fibrosis–HCC axis via bidirectional mechanisms. (1) In inflammation/fibrosis, FXR activation upregulates BSEP, FGF15/19, and SHP, inhibits CYP7A1 to maintain bile acid homeostasis, suppresses the TLR4/NF-κB axis and NLRP3 inflammasome, reduces IL-6/TNF-α, and directly inhibits hepatic stellate cell activation and matrix deposition. Agonists like INT-767 block progression from chronic hepatitis to fibrosis/cirrhosis (2) In HCC, FXR dysfunction (e.g., HBx C40-mediated). causes bile acid accumulation, glucose metabolic disorders, and Notch1/STAT3 activation, driving HCC progression. FXR activation inhibits STAT3 phosphorylation, glycolytic enzymes, and Wnt activity. Quercetin and obeticholic acid suppress tumor growth via FXR signaling. (3) Aberrant FXR signaling correlates with immune microenvironment dysregulation and immune escape. FXR agonists reshape the microenvironment and enhance anti-PD-1 efficacy; combined FXR and GPC3 detection improves HCC diagnostic specificity.</div></div><div><h3>Conclusion</h3><div>FXR is a central hub regulating the liver inflammation–fibrosis–HCC axis. FXR-targeting agonists, natural compounds, and combination immunotherapy hold significant translational potential. Further studies are needed to clarify FXR's tissue-specific functions and bidirectional mechanisms, and to develop highly selective modulators for precise liver disease prevention and treatment.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102753"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148854156","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":"KGTC-DDA:Drug-disease association prediction based on parallel graph isomorphism and transformer networks with cross-attention","authors":"Jiahao Chen,&nbsp;Zi Liu,&nbsp;Liyi Yu,&nbsp;Wang-Ren Qiu,&nbsp;Weizhong Lin,&nbsp;Xuan Xiao","doi":"10.1016/j.bbrep.2026.102766","DOIUrl":"10.1016/j.bbrep.2026.102766","url":null,"abstract":"<div><div>Drug development is a complex, time-consuming, and costly process, making drug repurposing an important strategy for identifying new therapeutic applications for existing drugs. Computational drug-disease association (DDA) prediction has therefore attracted increasing attention in recent years. Although many existing methods incorporate similarity information and graph neural networks for DDA prediction, effectively capturing both local structural patterns and global dependencies, as well as modeling complex interactions between drugs and diseases, remains challenging. To address these limitations, we propose Drug-disease association prediction model (KNN, GIN, Graph Transformer and Cross-attention, KGTC-DDA), a novel framework that combines Graph Isomorphism Networks (GIN), Graph Transformers (GT), and cross-attention mechanisms for drug-disease association prediction. Specifically, multiple biological similarities, including drug chemical structure similarity, disease phenotype similarity, and Gaussian interaction profile (GIP) kernel similarity, are integrated to construct comprehensive drug and disease similarity graphs. GIN and Graph Transformer modules are then employed in parallel to simultaneously learn local topological features and global contextual representations from the similarity networks. Furthermore, a cross-attention mechanism is introduced to capture high-order interdependencies between drug and disease embeddings, thereby enhancing heterogeneous feature interaction and representation learning. Extensive experiments on three benchmark datasets under 10-times 10-fold cross-validation demonstrate that KGTC-DDA achieves superior predictive performance compared with several state-of-the-art methods in terms of AUROC and AUPR. In addition, experiments on unseen disease prediction further validate the robustness and generalization capability of the proposed framework. These results indicate that KGTC-DDA provides an effective and promising approach for computational drug repositioning and drug-disease association prediction.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102766"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148958637","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":"A practical workflow for analyzing organelle spatial proximity with super-resolution microscopy.","authors":"Xiaoyu Ren, Ying Fan, Wenwen Jing, Junjing Yu","doi":"10.1016/j.bbrep.2026.102770","DOIUrl":"10.1016/j.bbrep.2026.102770","url":null,"abstract":"<p><p>Organelles establish dynamic contacts to facilitate inter-organelle communication. Although their structures and dynamics are commonly observed by light microscopy, the spatial precision of organelle proximity is restricted by optical diffraction limit. While super-resolution microscopy has significantly advanced the visualization of subcellular ultrastructure, optimizing imaging parameters and robust downstream analysis remains a key challenge. Here we present a practical workflow for live-cell super-resolution imaging and quantitative analysis of organelle spatial proximity. By combining super-resolution microscopy and machine learning-driven batch image processing, this method enables accurate estimation of organelle morphology and juxtapositions. Notably, this workflow is broadly adaptable to different subcellular structures, labeling strategies and imaging conditions. It is designed to be accessible to most cell biology laboratories without requiring large-scale training datasets or extensive computational resources.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"102770"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954733","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 central function and specific molecular mechanisms of the TLR4 pathway underlying impaired intestinal barrier in necrotizing enterocolitis","authors":"Xin Ren,&nbsp;Xiulan Su,&nbsp;Gaowa Arigong","doi":"10.1016/j.bbrep.2026.102754","DOIUrl":"10.1016/j.bbrep.2026.102754","url":null,"abstract":"<div><div>Neonatal necrotizing enterocolitisis a fatal gastrointestinal emergency affecting preterm infants, which is linked to destruction of intestinal barrier. The structural overexpression and negative regulation of Toll like receptor 4, a key receptor of lipopolysaccharidefrom Gram-negative bacteria in preterm intestinal epithelial cells, constitute a core hub connecting flora dysbiosis and barrier breakdown. When TLR4 neutrally binds with LPS, it signals the activation of the NF-κB-mediated inflammatory cascade through the MyD88/TRIF pathway which in turn induces apoptosis, necroptosis, and tight junction protein degradation in intestinal epithelial cells. degradation of tight junction protein of intestinal epithelial cells. The body naturally possesses protective mechanisms such as competitive receptors, intracellular negative regulatory networks, and microbial metabolites, which can be the target of drugs. Methods for the protection of the intestinal barrier by fine-tuning TLR4 signaling activity include small-molecule drugs, nano-delivery systems and nutritional interventions. Nonetheless, clinical translation remains hindered by the issues of TLR4 gene polymorphism, gestational age-dependent regulation, and immune balance maintenance. In the future, efforts should concentrate on the regulatory mechanisms of small molecule drugs and naturally occurring foodborne peptides. The goal is to combine the precision offered by genetic screening with a specific delivery system. This will allow for the targeted prevention and control of TLR4 signal systems. Ultimately, this will lead to a breakthrough in tackling the challenges associated with NEC treatment.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102754"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954717","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":"A recurrent CCDC82 frameshift variant associated with syndromic neurodevelopmental disorder in a consanguineous Pakistani family","authors":"Tehmeena Akhter,&nbsp;Sami Khan,&nbsp;Ahmed Abdul Mumeen,&nbsp;Muhammad Asif Naeem,&nbsp;Sheikh Riazuddin,&nbsp;Saima Riazuddin","doi":"10.1016/j.bbrep.2026.102764","DOIUrl":"10.1016/j.bbrep.2026.102764","url":null,"abstract":"<div><h3>Background</h3><div>Intellectual disabilities (IDs) are part of neurodevelopmental disorders (NDDs) and are genetically heterogeneous conditions characterized by impairments in cognition, learning, and adaptive functioning. Despite advances in gene discovery, many individuals, particularly those from understudied populations, remain without a molecular diagnosis. Recent reports implicate <em>CCDC82</em> (HGNC: 26282) as an autosomal recessive ID gene, although the phenotypic spectrum and biological context remain incompletely defined.</div></div><div><h3>Methods</h3><div>Exome sequencing (ES) was performed in a consanguineous Pakistani family (PKMR06A) with four affected individuals presenting with moderate to severe ID. Variant segregation was confirmed by Sanger sequencing. <em>In silico</em> analyses, including pathogenicity prediction, protein structural modeling, and domain intolerance assessment, were used to evaluate the functional consequences of the identified variant. Spatiotemporal gene expression patterns were examined using bulk and single-cell human brain transcriptomic datasets.</div></div><div><h3>Results</h3><div>Clinically, affected individuals of family PKMR06A presented with early childhood global developmental delay, speech delay, hypotonia, gait abnormalities, spasticity, and mild facial dysmorphism. Genetic screening revealed a recurrent rare homozygous frameshift variant in <em>CCDC82</em> (NM_024725.4): c.373del; p.(Asp125Ilefs*6), segregating with disease in all available affected individuals of the family. The identified c.373del variant was absent from the gnomAD database and was classified as pathogenic (PVS1, PM2, and PP1) based on ACMG/AMP criteria. The c.373del variant is predicted to introduce a premature termination codon, p.(Asp125Ilefs*6), leading to deletion of essential coiled-coil domains from the encoded protein, supporting a loss-of-function mechanism. <em>In silico,</em> transcriptomic analyses demonstrated preferential <em>CCDC82</em> expression during prenatal human brain development, providing developmental context for the neurodevelopmental phenotype associated with the identified truncating variant.</div></div><div><h3>Conclusions</h3><div>This study expands the mutational landscape of <em>CCDC82</em> and provides additional clinical and molecular evidence supporting its role in autosomal recessive NDD. The findings reinforce the importance of <em>CCDC82</em> in human neurodevelopment and highlight the value of genomic investigation in underrepresented populations.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102764"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954760","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":"From epigenetics to metastasis: Multifaceted roles of lncRNAs in gastric cancer","authors":"Mohamed J. Saadh,&nbsp;Ashok Kumar Bishoyi,&nbsp;R. Roopashree,&nbsp;K. Satyam Naidu,&nbsp;Lokesh Verma,&nbsp;Ojas Prakashbhai Doshi,&nbsp;Piyus Kumar Pathak,&nbsp;Suman Saini,&nbsp;Fadhil Faez Sead","doi":"10.1016/j.bbrep.2026.102761","DOIUrl":"10.1016/j.bbrep.2026.102761","url":null,"abstract":"<div><div>Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, largely due to its high metastatic potential and poor prognosis at advanced stages. Epithelial–mesenchymal transition (EMT) is a pivotal biological process that facilitates tumor invasion, dissemination, and therapeutic resistance in GC. In recent years, long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression, orchestrating multiple aspects of cancer progression through epigenetic, transcriptional, and post-transcriptional mechanisms. This review provides a comprehensive overview of the current understanding of lncRNA-mediated regulation of EMT and metastasis in gastric cancer. We summarize how lncRNAs function as epigenetic modulators, competing endogenous RNAs (ceRNAs), and molecular scaffolds to regulate EMT-associated transcription factors, signaling pathways, and chromatin dynamics. In particular, key oncogenic pathways such as Wnt/β-catenin, PI3K/AKT, STAT3, and NF-κB are highlighted as major downstream targets of lncRNA activity. Furthermore, we discuss the involvement of lncRNAs in tumor microenvironment remodeling, hypoxia response, angiogenesis, immune regulation, and extracellular matrix reorganization, all of which contribute to metastatic progression. Importantly, dysregulated lncRNA expression is closely associated with clinicopathological features and patient outcomes, underscoring their potential as diagnostic and prognostic biomarkers. In addition, the therapeutic targeting of lncRNAs represents a promising strategy for overcoming metastasis and treatment resistance in gastric cancer. Overall, this review integrates recent advances in the field and provides insights into the complex regulatory networks governed by lncRNAs, highlighting their translational potential in improving GC management.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"Article 102761"},"PeriodicalIF":3.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148958633","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":"Quantitative dot blot method for measuring EGFR protein levels in patients with colorectal cancer.","authors":"Ze Li, Na Li, Quanyong Li, Wenlei Xu, Guohua Yu, Wenguo Jiang","doi":"10.1016/j.bbrep.2026.102756","DOIUrl":"10.1016/j.bbrep.2026.102756","url":null,"abstract":"<p><strong>Purpose: </strong>The expression levels of the epidermal growth factor receptor (EGFR) may be associated with the efficacy of cetuximab (CTX); however, conventional immunohistochemical assays lack quantitative accuracy and standardization, thereby making it hard to achieve absolute quantification of protein expression and cross-platform comparisons. To establish an objective quantitative standard for EGFR protein expression levels, we employed quantitative dot blotting (QDB) to analyze tumor samples from patients with RAS/BRAF wild-type colorectal cancer (CRC).</p><p><strong>Materials and methods: </strong>We collected 89 formalin-fixed, paraffin-embedded (FFPE) tumor tissue specimens from patients with CRC stored at Yuhuangding Hospital in Yantai for QDB testing. Of these, 42 served as untreated controls, and 47 patients received CTX treatment.</p><p><strong>Results: </strong>EGFR protein levels in all patients with CRC ranged from 0.05 to 3.85 nmol/g (n = 89). Using the predefined cohort-wide cutoff of 0.23 nmol/g, a chi-square test performed using the Statistical Package for the Social Sciences software revealed that patients with low EGFR expression had longer overall survival, regardless of CTX treatment.</p><p><strong>Conclusions: </strong>This study established a QDB-based assay capable of quantitatively and objectively measuring EGFR protein levels in CRC specimens. This assay helps establish the value of EGFR protein as a predictive biomarker and is expected to assist in the retrospective and prospective evaluation of anti-EGFR therapies in clinical trials.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"47 ","pages":"102756"},"PeriodicalIF":3.3,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954726","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}