Biomolecules & biomedicine最新文献

{"title":"Function and mechanism of miRNAs during the process of <i>Klebsiella pneumoniae</i> infection.","authors":"Chuhan Zhang, Ge Li, Safi Ullah, Liang Liu, Huajie Zhao, Fan Yang, Liwei Guo, Duan Li","doi":"10.17305/bb.2025.11421","DOIUrl":"https://doi.org/10.17305/bb.2025.11421","url":null,"abstract":"<p><p>Klebsiella pneumoniae (K. pneumoniae), a Gram-negative bacterium, is a major cause of nosocomial infections and can lead to severe, widespread infections. The rise of hypervirulent and multidrug-resistant K. pneumoniae presents significant challenges to public health. Diseases associated with K. pneumoniae, such as pneumonia, lung injury, peritonitis, and sepsis, have garnered increasing attention. MicroRNAs (miRNAs) are a class of short, endogenously expressed non-coding RNAs that regulate gene expression by inhibiting translation or promoting mRNA degradation. As key regulators of gene expression, miRNAs play a crucial role in K. pneumoniae infections by modulating host inflammatory pathways, suppressing inflammasome activity, regulating cytokine secretion, and facilitating post-translational modifications. Understanding miRNA alterations and their mechanisms during K. pneumoniae infections is of great significance. This comprehensive review explores the functions and mechanisms of miRNAs in K. pneumoniae-induced lung injury, peritonitis, and sepsis. By analyzing differential miRNA expression during infection, we aim to provide new insights and potential directions for future clinical diagnosis and treatment strategies for K. pneumoniae infections.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537870","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":"Advancing ICU mortality prediction in community-acquired pneumonia: Combining fibrinogen-to-albumin ratio, CT severity score, PSI, and CURB-65.","authors":"Ece Unal Cetin, Ozge Kurtkulagi, Fatih Kamis, Murat Das, Esen Simsek, Adil Ugur Cetin, Yavuz Beyazit","doi":"10.17305/bb.2025.12127","DOIUrl":"https://doi.org/10.17305/bb.2025.12127","url":null,"abstract":"<p><p>Community-acquired pneumonia (CAP) is a leading cause of ICU admissions, with significant morbidity and mortality. Traditional risk stratification tools, such as CURB-65, the pneumonia severity index (PSI), and computed tomography severity scores (CT-SS) are widely used for prognosis but could be improved by incorporating novel biomarkers. This retrospective study evaluated the fibrinogen-to-albumin ratio (FAR) as an additional predictor of 30-day mortality in ICU patients with CAP. A total of 158 CAP patients admitted to a tertiary care ICU were included. Baseline data encompassed demographic, clinical, laboratory, and radiological parameters, including FAR, CURB-65, PSI, and CT-SS. Logistic regression and receiver operating characteristic curve (ROC) analyses were conducted to assess mortality predictors. The 30-day mortality rate was 70.88% (112/158). Higher FAR, PSI, CURB-65, CT-SS, and lactate levels were independently associated with increased mortality (P < 0.05). FAR demonstrated strong discriminatory power (area under the receiver operating characteristic [AUROC]: 0.704) and significantly improved the predictive accuracy of established models. Adding FAR to PSI increased the AUROC from 0.705 to 0.791 (P = 0.009), while combining FAR, CT-SS, and PSI yielded the highest predictive accuracy (AUROC: 0.844, P = 0.032). These findings suggest that FAR, which reflects both inflammation and nutritional status, complements traditional risk assessment tools by providing a dynamic perspective. Integrating FAR into existing models enhances the identification of high-risk patients, enabling timely interventions and more efficient resource allocation in the ICU.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560172","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 regulatory role of exercise in heart failure and myocardial energy metabolism: A review.","authors":"Yuanhao Li, Dongli Gao, Peixia Li, Xulei Duan, Youli Liu, Chengyan Wu, Libo Wang, Xuehui Wang","doi":"10.17305/bb.2025.12072","DOIUrl":"https://doi.org/10.17305/bb.2025.12072","url":null,"abstract":"<p><p>Myocardial energy metabolism is crucial for maintaining optimal heart function. The heart, having limited energy storage capacity, is dependent on a continuous energy supply; any disruptions or alterations in energy metabolism pathways can lead to insufficient myocardial energy, potentially triggering heart failure (HF). Exercise, as a safe and economical non-pharmacological intervention, is widely recognized to enhance cardiovascular health and modify myocardial energy metabolism patterns. However, the specific mechanisms by which exercise regulates myocardial metabolism to prevent and treat HF remain unclear. This review aims to detail the characteristics of myocardial metabolism under normal physiological and HF conditions, to further explore the impact of different exercise modalities on myocardial metabolism, and to summarize the molecular mechanisms by which exercise protects the heart by optimizing myocardial energy metabolism. Ultimately, this article aims to provide an in-depth understanding and evidence for the application of exercise interventions in cardiac rehabilitation.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560204","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":"miR-542-3p attenuates corticosterone-induced hippocampal neuronal damage in depressive mice by modulating PTEN/AKT/GSK3β/β-catenin pathway.","authors":"Ningbo Yang, Jie Li, Hongxia Hu, Xujiang Wang","doi":"10.17305/bb.2025.11523","DOIUrl":"https://doi.org/10.17305/bb.2025.11523","url":null,"abstract":"<p><p>Depression is a common psychological disease, and nerve injury is the key link of depression. The molecular mechanism involved in this link needs to be explored. miR-542-3p can reduce the degree of hippocampal neuronal damage in rats, but its mechanism in the neural damage of depression is still unclear. HT-22 cell injury was induced by corticosterone (CORT). After overexpression or knockdown of miR-542-3p, CORT-induced HT-22 cell injury was tested by cell counting kit-8 (CCK-8) assay, lactate dehydrogenase (LDH) assay and flow cytometry. Inflammatory and oxidative stress indicator levels were analyzed by kit and flow cytometry. The target genes of miR-542-3p were obtained by database analysis, and the targeting relationship between miR-542-3p and phosphatase and tensin homolog (PTEN) was explored based on dual luciferase assay. After PTEN overexpression or application of AKT pathway agonist MK-2206, the degree of cell damage, inflammation, and oxidative stress were detected again. CORT was used to induce depression in mice. Pathological changes of brain tissue structure and neuronal survival were observed by pathological staining. The miR-542-3p, PTEN, and AKT/GSK3β/β-catenin pathway protein levels in vivo and in vitro were detected by qRT-PCR and Western blot. Overexpression/knockdown of miR-542-3p alleviated/aggravated CORT-induced cell injury, inflammation, and oxidation levels in HT-22 cells (P < 0.05). Meanwhile, overexpressed miR-542-3p can reduce neurological damage of mice. miR-542-3p can target PTEN, and it can trigger the AKT/GSK3β/β-catenin pathway by targeting PTEN expression to reduce CORT-induced nerve injury (P < 0.05). miR-542-3p can reduce CORT-induced hippocampal neuronal damage by targeting PTEN and activating the AKT/GSK3β/β-catenin pathway.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569035","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 MITF expression on tumor-infiltrating lymphocytes in melanoma: Insights into immune microenvironment dynamics.","authors":"Damir Vučinić, Matea Lekić, Gordana Žauhar, Gordana Zamolo","doi":"10.17305/bb.2025.12125","DOIUrl":"https://doi.org/10.17305/bb.2025.12125","url":null,"abstract":"<p><p>Melanoma progression is influenced by complex interactions between tumor cells and the immune microenvironment. This study examined the relationship between microphthalmia-associated transcription factor (MITF) expression and the immune microenvironment in primary melanoma using a modified classification of tumor-infiltrating lymphocytes (TILs) based on conventional BRISK categories. Archival formalin-fixed, paraffin-embedded tissue samples from 81 primary melanoma patients were analyzed via tissue microarray immunohistochemistry to assess MITF protein levels. TIL patterns were categorized into six groups, refining the traditional BRISK classification to distinguish between continuous and discontinuous infiltration, as well as peripheral vs intratumoral distribution. The analysis revealed that melanomas classified under the BRISK B category exhibited the highest MITF expression, often exceeding 50%. In contrast, tumors in the NON-BRISK and ABSENT TIL groups showed significantly lower MITF expression (mean values: 32.73% ± 16.98% and 22.00% ± 10.54%, respectively), with statistically significant differences (Kruskal-Wallis test, P = 0.027; modified classification, P = 0.011). Additionally, the presence of CD20+ B lymphocytes correlated with increased MITF expression (P = 0.009). MITF gene amplification was detected in 29% of cases, though its association with protein expression showed only a trend (P = 0.058). These findings highlight the complex interplay between MITF expression and TIL distribution in melanoma, suggesting that refined TIL classification may offer deeper insights into tumor immunobiology and help predict responses to immunotherapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460957","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":"Lymphocyte subsets predict mortality in acute paraquat poisoning.","authors":"Qian Dong, Huan Xu, Pengjie Xu, Jiang Liu","doi":"10.17305/bb.2025.11891","DOIUrl":"https://doi.org/10.17305/bb.2025.11891","url":null,"abstract":"<p><p>Paraquat (PQ) is a highly effective herbicide widely used in agricultural production, known for its strong herbicidal power, rapid action, and minimal environmental pollution. However, it is also highly toxic to humans and animals, with acute lung injury (ALI) being the primary cause of death. While the toxic mechanisms of PQ have been studied from various perspectives, its effects on lymphocytes and their subsets remain unclear. This study aimed to explore the relationship between lymphocyte dysfunction and mortality in acute PQ poisoning. A total of 92 patients with PQ poisoning who visited the emergency department of The Affiliated Lihuili Hospital of Ningbo University between January 1, 2016, and September 30, 2021, were included. Basic demographic and laboratory data within 24 h of admission were collected. Peripheral blood lymphocyte subsets were analyzed using flow cytometry. To identify independent risk factors for mortality, patients were followed up for 90 days. COX proportional hazards models and LASSO regression were applied to screen for predictive variables and develop a predictive model. All participants provided informed consent, and the study was approved by the relevant ethics committee. Among the 92 patients, 36 died. Compared with the survival group, the death group showed significantly higher white blood cell and neutrophil counts, lymphocyte counts, and CD4+/CD8+ T cell ratios, while the percentage of natural killer (NK) cells was significantly lower (P < 0.001). COX regression analysis identified these factors as independent risk factors for mortality: lymphocyte count: hazard ratio (HR) = 1.59; 95% confidence interval (CI), 1.02-2.47; P = 0.04 neutrophil count: HR = 1.12; 95% CI, 1.06-1.18; P = 0.04 CD4+/CD8+ T cell ratio: HR = 2.01; 95% CI, 1.03-3.92; P = 0.04 NK cell percentage: HR = 0.88; 95% CI, 0.82-0.95; P = 0.002. These findings suggest that lymphocyte count, neutrophil count, CD4+/CD8+ T cell ratio, and NK cell percentage are all associated with mortality in PQ poisoning cases.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460892","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":"Study on the mechanism of Wnt/β-catenin pathway mediated by pterostilbene to reduce cerebral ischemia-reperfusion injury.","authors":"Yang Jin, Chunwang Fu, Ming Guo, Qiang Yang","doi":"10.17305/bb.2025.11743","DOIUrl":"https://doi.org/10.17305/bb.2025.11743","url":null,"abstract":"<p><p>Cerebral ischemia-reperfusion injury (CIRI) is the primary cause of damage following ischemic stroke, with ferroptosis serving as a key pathophysiological factor in CIRI. Pterostilbene (PTE) has been shown to reduce cerebral ischemic injury, but whether its mechanism of action involves ferroptosis remains unclear. In this study, an in vitro model of mouse hippocampal neuron (HT22) cell injury and an in vivo mouse CIRI model were established. Treatments included PTE, the ferroptosis activator Erastin, and the Wnt signaling pathway inhibitor (Dkk-1). Cell damage was assessed using flow cytometry, MTT assay, lactate dehydrogenase (LDH) release assay, and Calcein-AM/PI staining. Oxidative stress and ferroptosis in cells and tissues were evaluated using biochemical kits and fluorescence staining. Additionally, histopathological staining was performed to assess brain tissue damage, while qRT-PCR and Western blot analyses were used to measure ferroptosis-related factors and Wnt/β-catenin pathway-related proteins in both cells and tissues. HT22 cells subjected to injury exhibited decreased viability and increased cell death (P < 0.05). Similarly, CIRI mice demonstrated pronounced cerebral infarction and neuronal damage. Ferroptosis, characterized by elevated levels of iron ions, lipid peroxides (ROS and MDA), and reduced antioxidant enzymes (GSH and GPX4), was significantly increased in both cells and tissues (P < 0.05). Correspondingly, ferroptosis-related protein levels were elevated (P < 0.05), while Wnt/β-catenin pathway-related protein levels were significantly decreased (P < 0.05). Treatment with Erastin and Dkk-1 exacerbated neuronal damage, intensified ferroptosis, and inhibited the Wnt/β-catenin pathway. Conversely, PTE treatment activated the Wnt/β-catenin pathway, reduced ferroptosis, and improved neuronal damage. Specifically, PTE upregulated the Wnt/β-catenin pathway, decreased peroxide accumulation, and antagonized ferroptosis, ultimately mitigating CIRI. These findings suggest that PTE protects against CIRI by modulating the Wnt/β-catenin pathway and alleviating ferroptosis-induced damage.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460902","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":"<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":"https://doi.org/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":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470258","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":"Methylene blue mitigates lung injury in HCA rats by regulating macrophage pyroptosis via Nrf2/HO-1 and NLRP3 pathways.","authors":"Fuyan Ding, Hong Wang, Gang Qiao, Zhidong Zhang","doi":"10.17305/bb.2025.11851","DOIUrl":"https://doi.org/10.17305/bb.2025.11851","url":null,"abstract":"<p><p>Methylene blue (MB) has antioxidant properties, yet its role in acute lung injury (ALI) induced by hypothermic circulatory arrest (HCA) remains unexplored. This study investigates MB's effects and underlying regulatory mechanisms in an HCA rat model. Rats received an intravenous bolus of MB (1 mg/kg) 15 min before HCA induction. Physiological parameters were monitored, and bronchoalveolar lavage fluid (BALF) was collected 2 h postoperatively to assess total protein levels, inflammatory cells, and cytokines. Histopathological lung damage was evaluated using hematoxylin-eosin (H&E) and TUNEL staining. Inflammatory markers and oxidative stress indicators were measured via ELISA and dihydroethidium (DHE) staining. Alveolar macrophages (AMs) were isolated to analyze polarization using flow cytometry and immunofluorescence double staining. Pyroptosis in AMs was detected with Yo-Pro-1 and Hoechst 33342 staining. Additionally, Western blotting was performed to examine the nuclear factor erythroid-2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, Nod-like receptor protein 3 (NLRP3) inflammasome, and pyroptosis-related proteins. Following HCA, rats exhibited significant blood gas abnormalities, structural lung damage, increased pathological scores, and higher apoptosis rates. However, MB mitigated these effects, improving physiological parameters and reducing lung histopathology scores. MB also lowered proinflammatory cytokine levels, increased SOD and GSH-Px activity, promoted AM polarization toward the M2 phenotype, and decreased pyroptosis. Mechanistically, MB activated the Nrf2/HO-1 pathway while inhibiting NLRP3 inflammasome activation. Notably, Nrf2 inhibitors and NLRP3 agonists weakened MB's protective effects by promoting inflammasome activation and pyroptosis, whereas Nrf2 agonists and NLRP3 inhibitors enhanced MB's beneficial impact. In conclusion, MB attenuates HCA-induced ALI by modulating AM polarization and pyroptosis via Nrf2/HO-1 pathway activation and NLRP3 inflammasome inhibition.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434557","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":"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":"https://doi.org/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":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400864","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}