Background Infantile pneumonia is a common health concern worldwide, with elevated morbidity and mortality rates among affected children. This study aims to identify key genes associated with infantile pneumonia using bioinformatics and unravel the underlying mechanisms. Results OLFM4 was the only biomarker identified for infantile pneumonia. Besides, OLFM4 expression was promoted in the serum of infantile pneumonia patients, and LPS-stimulated cells and mouse models. OLFM4 knockdown repressed cell apoptosis, levels of TNF-α, IL-6, IL-1β, MPO, MDA, ROS, and activation of the NF-κB pathway, and facilitated the SOD level in LPS-induced models. OLFM4 knockdown alleviated the lung injury of the LPS-induced mouse model. Conclusions OLFM4 knockdown alleviated cell apoptosis, inflammatory response, and oxidative stress via the NF-κB signaling pathway in LPS-induced WI-38 cells and mouse model. The findings suggest that OLFM4 may pave the way for the treatment of infantile pneumonia.How to cite: Wu Y, Cao B, Liu J. Exploration of OLFM4 as a biomarker for infantile pneumonia and underlying mechanisms via bioinformatics, machine learning algorithms, and LPS-induced models. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100719.
Background Arrhythmia refers to a disorder in which abnormal cardiac electrical activity leads to irregular heart rhythm and conduction. Resveratrol (Res), a natural polyphenol compound extracted from medicinal plants, plays an important role in the treatment of arrhythmia, but its precise molecular mechanisms remain unclear. Results The intersection of Res targets and arrhythmia yielded 78 common targets, including F-box protein 32 (FBXO32). These targets were significantly enriched in cardiac conduction system development, protein-containing complex, vascular endothelial growth factor (VEGF) signaling pathway, cyclic adenosine monophosphate (cAMP) signaling pathway, and forkhead box O (FoxO) signaling pathway. Molecular docking confirmed that FBXO32 could stably bind to Res. Res treatment increased cell viability in the arrhythmia cell model. FBXO32 was highly expressed in the arrhythmia cell model, but its expression was significantly reduced under Res treatment. Knockdown of FBXO32 increased cell viability, decreased apoptosis, and increased protein levels of calcium voltage-gated channel subunit alpha1 C (CACNA1C) and human ether-à-go-go-related gene (hERG), whereas Res treatment partially modulated these effects. Conclusions Res inhibits the expression of FBXO32, thereby suppressing the malignant phenotypes of arrhythmia.How to cite: Lou X, Huang L, Wen N, et al. Molecular targets and mechanisms of resveratrol in alleviating arrhythmia based on network pharmacology and bioinformatics. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100720.
Background Vitiligo is a common depigmentation disorder that affects approximately 1–2% of the global population. Oxidative stress plays a crucial role in its pathogenesis, yet systematic identification of oxidative stress-related biomarkers remains limited. This study aimed to identify and validate oxidative stress-related biomarkers for vitiligo and to construct a risk prediction model using bioinformatics, machine learning, and Mendelian randomization approaches. Results Through integration of high-throughput sequencing data, 1,581 differentially expressed genes were identified, of which 42 intersected with known oxidative stress-related genes. Three machine learning algorithms converged on five candidate genes. Real-time polymerase chain reaction validation in paired vitiligo lesional and non-lesional skin tissues confirmed the significant upregulation of ATOX1, STAT1, and PDCD10 and downregulation of FXN (p < 0.05). A risk prediction nomogram based on these four genes achieved high accuracy in the training dataset (area under the curve = 1.00) and an independent validation dataset (area under the curve = 0.93). PDCD10 demonstrated the strongest individual discriminatory performance (area under the curve = 0.820) in external validation. Mendelian randomization analysis indicated that ATOX1, STAT1, and PDCD10 had odds ratios greater than 1, suggesting a potential trend toward increased vitiligo risk, although the associations did not reach statistical significance. Conclusions This study identified ATOX1, STAT1, FXN, and PDCD10 as oxidative stress-related biomarkers for vitiligo. The four-gene risk prediction model demonstrated promising accuracy, with potential implications for early detection and personalized treatment strategies, pending further validation in larger cohorts.How to cite: Xia Y, Liu L, Zhou H, et al. Oxidative stress gene signature associated with vitiligo: A multi-algorithm machine learning and Mendelian randomization validation. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100724.
Background Colonic mucinous adenocarcinoma is a highly aggressive subtype of colon cancer. Epidemiological evidence has linked estrogen exposure to certain gastrointestinal malignancies, yet its pathophysiological role in the pathogenesis of colonic mucinous adenocarcinoma remains unclear. This study aimed to investigate the effect of estrogen on tumor growth in a rat model of colonic mucinous adenocarcinoma and its association with intestinal mucosal epithelial proliferation-related factors and apoptosis. Results Compared with the normal control group, the model control group showed significantly increased tumor proliferative activity and elevated intestinal epithelial apoptosis. After estrogen intervention, tumor volume and proliferative activity were inhibited, the expressions of Ki-67 and proliferating cell nuclear antigen were downregulated, and the apoptosis rate of intestinal epithelial cells decreased; an estrogen antagonist could enhance some of the above effects. Conclusions Estrogen can slow the growth of colonic mucinous adenocarcinoma by inhibiting intestinal mucosal epithelial proliferation, exhibiting potential anti-tumor effects. Its mechanism may be related to regulating the proliferation-apoptosis balance of intestinal mucosal epithelium, providing experimental evidence for colon cancer therapy research.How to cite: Wang K, Yue Y, Liu X, et al. Estrogen attenuates colonic mucinous adenocarcinoma growth in a rat model by inhibiting proliferation and promoting apoptosis. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100725.
Background The industrial production of alginate lyase provides high-quality tool enzymes for the enzymatic hydrolysis of large brown algae. Establishing a seaweed enzymatic hydrolysis process that is simple to operate while offering both high enzymatic hydrolysis efficiency and a high yield of oligosaccharides contributes to the high-value utilization of large brown algae. Results A one-step enzymatic hydrolysis process combining alginate lyase, pectinase and cellulase was adopted to conduct enzymatic hydrolysis experiments on Sargassum horneri and Saccharina japonica, respectively. The Box-Behnken experimental design was applied to optimize the dosage of the three enzymes, as well as the temperature, pH and reaction time of enzymatic hydrolysis. The results showed that the optimal enzymatic hydrolysis conditions for S. horneri were as follows: alginate lyase 490 U/g, pectinase 4660 U/g, cellulase 380 U/g, hydrolysis temperature 47°C, hydrolysis pH 5.5 and hydrolysis time 8 h. For S. japonica, the optimal enzymatic hydrolysis conditions were alginate lyase 360 U/g, pectinase 5000 U/g, cellulase 284 U/g, hydrolysis temperature 49.5°C, hydrolysis pH 5.2 and hydrolysis time 8.8 h. After process optimization, the solid hydrolysis rates of S. horneri powder and S. japonica powder were increased to 71.4% and 66.3%, respectively, and the proportion of low-molecular-weight alginate oligosaccharides (DP < 6) in the hydrolysates reached approximately 70%; both enzymatic hydrolysates exhibited favorable antioxidant activity according to the detection. Conclusions The findings of this study greatly simplify the technological process for preparing alginate oligosaccharides via brown algae enzymatic hydrolysis and significantly improve the production efficiency.How to cite: Shi K, Dong Y, Wang Q, et al. Optimization of one-step enzymatic hydrolysis conditions for two large brown algae and analysis of the antioxidant activity of the hydrolysis products. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100722.
Background Diabetic retinopathy is characterized by excessive microvascular proliferation that leads to vitreous hemorrhage, retinal traction, and subsequent visual impairment. Aberrant expression of IGF2BP3 is involved in the pathogenesis of multiple diseases. This study aimed to elucidate the mechanism by which IGF2BP3 mediates diabetic retinopathy by regulating semaphorin-3G (SEMA3G) expression. Results Elevated IGF2BP3 expression was observed in diabetic retinopathy. In vitro, IGF2BP3 overexpression promoted pathological angiogenesis, whereas its knockdown significantly attenuated wound healing, reduced inflammatory cytokine secretion, and suppressed cellular proliferation. A targeted regulatory relationship between IGF2BP3 and SEMA3G mRNA was identified, with IGF2BP3 enhancing SEMA3G mRNA stability. SEMA3G was upregulated in diabetic retinopathy, and its overexpression partially rescued the diabetic retinopathy progression suppressed by IGF2BP3 silencing. In vivo, IGF2BP3 overexpression aggravated histopathological alterations, thereby accelerating diabetic retinopathy development. Conclusions In summary, IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability.How to cite: Chen Y, Zhao T, Han M, et al. IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability. Electron J Biotechnol 2026;83. https://doi.org/10.1016/j.ejbt.2026.100723.
Background: Diabetic retinopathy is a major microvascular complication of diabetes and a leading cause of vision loss. Persistent low-grade inflammation drives disease progression. Pyroptosis, characterized by its pro-inflammatory nature, is involved in several inflammatory diseases, yet the molecular mechanisms specific to diabetic retinopathy remain largely undefined. This study aimed to identify the key molecular drivers and regulatory pathways of pyroptosis in diabetic retinopathy. Results: Five key pyroptosis-related genes were identified: ubiquitin-specific peptidase 24, signal transducer and activator of transcription 3, and ABL proto-oncogene 1 were upregulated, while tripartite motif containing 24 and tubulin beta 6 class VI were downregulated in diabetic retinopathy. High glucose exposure induced pyroptotic morphology and increased lactate dehydrogenase, interleukin-1 beta, and interleukin-18 levels. Functional assays demonstrated that ABL proto-oncogene 1 acts upstream of signal transducer and activator of transcription 3 to activate the NOD-like receptor family pyrin domain-containing 3 inflammasome, ultimately leading to pyroptosis. Signal transducer and activator of transcription 3 showed strong diagnostic value with an area under the curve exceeding 0.9. Conclusions: This study identifies a novel ABL proto-oncogene 1–signal transducer and activator of transcription 3–NOD-like receptor family pyrin domain containing 3 signaling axis as a central regulator of pyroptosis in diabetic retinopathy. These findings provide insights into inflammation-induced retinal pathology and suggest candidate molecular targets for therapeutic intervention.How to cite: Hu L, Chen G, Pan H, et al. ABL1-STAT3-NLRP3 axis attenuates pyroptosis and alleviates diabetic retinopathy. Electron J Biotechnol 2026;82. https://doi.org/10.1016/j.ejbt.2026.100717.
Background: Non-small cell lung cancer (NSCLC) represents the top contributor to cancer-associated deaths globally, and its suboptimal clinical outcomes are linked to late-stage detection and acquired resistance to existing therapies. Microrchidia family CW-type zinc finger 2 (MORC2) has been found to exhibit oncogenic potential in NSCLC, but its transcriptional regulatory mechanisms and role in glycolytic reprogramming remain unclear. Results: As a key gene, MORC2 was found to be overexpressed in NSCLC and linked to poor prognosis. MORC2 silencing impaired cell proliferation, stemness, and invasion, diminished glycolysis, and enhanced apoptosis. PAX2 was confirmed to directly transcriptionally activate MORC2; overexpression of MORC2 reversed the defects in malignant phenotypes induced by PAX2 knockdown. In vivo, depletion of PAX2 suppressed tumor growth, which was partially rescued by MORC2 overexpression. Conclusions: The PAX2/MORC2 axis was demonstrated to drive NSCLC malignancy, supporting MORC2 as a potential prognostic marker and therapeutic target for NSCLC.How to cite: Cao J, Cai F, Jia J, et al. Identification of MORC2 via bioinformatics and machine learning reveals its transcriptional activation by PAX2 in NSCLC malignancy. Electron J Biotechnol 2026;82. https://doi.org/10.1016/j.ejbt.2026.100718.
Background: Lung cancer (LC) remains the leading cause of cancer-related mortality. While the traditional formula Wenyang Hualiu Tang (WYHLT) has shown efficacy against LC, the role of adenylate uridylate (AU)-rich element (ARE)-related genes (AREGs) in this disease and its treatment is unexplored. This study aimed to elucidate the mechanism by which AREGs are involved in WYHLT treatment of LC. Results: Transcriptome sequencing of a mouse LC model with WYHLT intervention (low, medium, high dose) identified four key biomarkers: GREB1, MUC2, NPTX2, and PPIP5K1. Enrichment analysis linked MUC2, NPTX2, and PPIP5K1 to translation. A constructed regulatory network revealed interactions involving three biomarkers (PPIP5K1, GREB1, NPTX2), 16 long non-coding RNAs (lncRNAs), and 10 circular RNAs (circRNAs), with lncRNA Malat1 targeting four microRNAs (miRNAs). Drug prediction analysis identified seven drugs targeting MUC2 and one targeting NPTX2, with PD-98059 showing the highest binding affinity for MUC2. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) vali-dation confirmed that WYHLT intervention increased PPIP5K1 and MUC2 expression and decreased GREB1 and NPTX2 expression compared to the LC model. Conclusions: This study identifies GREB1, MUC2, NPTX2, and PPIP5K1 as potential biomarkers involved in WYHLT treatment of LC. The findings provide new insights into the molecular mechanisms of WYHLT and novel directions for LC therapeutic research. (c) 2026 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Val-para & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Background: Gastric cancer is a highly prevalent and lethal malignancy worldwide, with its immune microenvironment playing a crucial role in tumor initiation and progression. Among selenoproteins, glutathione peroxidase 3 (GPX3) is an important antioxidant enzyme that has recently attracted attention for its roles in various cancers. However, the function of GPX3 and its impact on the immune microenvironment in stomach adenocarcinoma (STAD) remain insufficiently explored. Results: Deep STAD tissues were more enriched in immune cells compared to superficial tumor tissues, particularly myeloid cells and fibroblasts. GPX3 was predominantly expressed in fibroblasts and myeloid cells, while its expression in T cells was relatively low, with no significant differences across different tumor layers. Moreover, GPX3 exhibited weak correlations with PD-1 and CTLA-4, suggesting that GPX3 may not directly mediate immune evasion via immune checkpoint pathways. These findings characterize the cellular distribution of GPX3 within the STAD immune microenvironment and provide initial insights into its potential regulatory function. Conclusions: Although GPX3 may not directly influence immune checkpoint pathways, its high expres-sion in myeloid cells and fibroblasts suggests that it might indirectly modulate immune responses by reg-ulating the tumor microenvironment. These results lay a theoretical foundation for future research on GPX3 in gastric cancer and its potential as a therapeutic target. How to cite: Shao Y, Cui S, Zhang C, et al. Glutathione peroxidase 3 as a predictor of immune modulation in gastric adenocarcinoma. Electron J Biotechnol 2026;81. https://doi.org/10.1016/j.ejbt.2026.100713. (c) 2026 Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Background: Periodontitis is a chronic inflammatory disease characterized by progressive alveolar bone loss. This study explored the role of exosomes derived from periodontal ligament stem cells (PDLSCs-Exo) in repairing alveolar bone defects in periodontitis. Results: PDLSCs-Exo significantly promoted new bone formation and collagen deposition in the defect area while reducing pro-inflammatory factors and enhancing M2 macrophage polarization. The knockdown of semaphorin 4D (SEMA4D) or plexin B1 (PLXNB1) further enhanced exosome-mediated repair, whereas their overexpression attenuated it. Additionally, the upregulation of PLXNB1 reversed the reparative effects of SEMA4D downregulation on alveolar bone defects in periodontitis. Conclusions: PDLSCs-Exo promotes M2 macrophage polarization by inhibiting the SEMA4D/PLXNB1 axis, alleviating local inflammation and accelerating alveolar bone defect repair in periodontitis. This finding provides a novel theoretical basis for the clinical treatment of periodontitis-related alveolar bone defects and identifies potential therapeutic targets for improving the efficacy of bone defect repair. How to cite: Yang Y, Zhang C. Periodontal ligament stem cell-derived exosomes promote alveolar bone defect repair in periodontitis by mediating M2 macrophage polarization via regulation of the SEMA4D/ PLXNB1 axis. Electron J Biotechnol 2026;81. https://doi.org/10.1016/j.ejbt.2026.100712. (c) 2026 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Background: In-situ straw return is an effective agronomic practice for improving soil quality and increasing crop yields. However, in Northeast China, prolonged seasonal freezing lasting more than 6 months markedly restricts straw decomposition, thereby limiting the benefits of straw return in saline-alkali soils. To overcome this constraint, cold-tolerant bacterial agents were applied to promote the decomposition and in-situ return of rice straw under frozen and low-temperature conditions. Results: The results demonstrated that under freezing and low-temperature conditions, the application of the microbial agent (CF) increased the rice straw decomposition rate to 51.22%, which was significantly higher than that observed in the control treatment (34.64%). The germination index of seeds exposed to the decomposed straw reached 102.87%, indicating that the decomposition products met safety standards. CF treatment reduced rhizosphere soil pH and salinity, while significantly increasing the diversity and abundance of rhizosphere microorganisms. In particular, it promoted the enrichment of bacterial genera associated with nitrogen fixation and straw decomposition. At the same time, the CF application enhanced rhizosphere soil nutrient levels, which in turn significantly improved rice growth parameters,including tiller number, plant height, and dry weight. Consequently, rice yield increased by 5.84% com-pared with the control treatment. Conclusions: In summary, the application of cold-tolerant bacterial agents enables efficient in-situ decom-position and return of rice straw under freezing and low-temperature conditions. This approach effec-tively enhances rice productivity in saline-alkali farmland and provides a simple, practical, and scalable strategy for overcoming straw decomposition limitations in cold regions worldwide. How to cite: Yang B, Zong X, Lin L, et al. Study on the effect of catalytic rotting and returning of rice straw to the field on rhizosphere soil and rice yield. Electron J Biotechnol 2026;81. https://doi.org/10.1016/j. ejbt.2026.100711. (c) 2026 The Authors. Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpar-a & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/ by-nc-nd/4.0/).
Background: Cutaneous melanoma (CM) is a highly aggressive skin malignancy with marked molecular heterogeneity and poor prognosis. Pyroptosis, an inflammatory form of programmed cell death, has been implicated in tumor progression and immune regulation; however, its prognostic value in CM remains incompletely understood. Results: Gene expression data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas skin cutaneous melanoma (TCGA-SKCM) cohorts were analyzed to identify pyroptosis-related differentially expressed genes (PRGs). Eight CM-associated PRGs were identified through integrated differential expression and intersection analyses. Functional enrichment analyses revealed that these genes were involved in inflammatory responses, immune regulation, and cell cycle-related pathways. A prognostic model was constructed using univariate Cox and least absolute shrinkage and selection operator (LASSO) regression analyses in the TCGA-SKCM cohort. Six PRGs were incorporated into the prognostic signature, of which ISG15, GZMB, and EGFR were independently associated with patient survival. The model demonstrated good predictive performance, as confirmed by receiver operating characteristic curves, Kaplan-Meier survival analysis, calibration plots, and decision curve analysis at 1-, 3-, and 5-year time points. Immune infiltration analysis revealed that ISG15, GZMB, and EGFR expression were positively correlated with the enrichment of multiple immune cell populations. Mutation profiling further supported the clinical relevance of these prognostic genes. Conclusions: In summary, we developed a pyroptosis-related prognostic model for cutaneous melanoma and identified ISG15, GZMB, and EGFR as clinically relevant prognostic biomarkers. Our findings enhance the understanding of pyroptosis-associated molecular mechanisms in CM and support their potential utility in prognostic stratification. How to cite: Jiang Y, Chen Y, Gao S, et al. Identification and validation of a pyroptosis-relevant model for the prognosis of cutaneous melanoma. Electron J Biotechnol 2026;81. https://doi.org/10.1016/j.ejbt.2026. 100709. (c) 2026 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Background: It is reported that matrisome exerts a significant function in the pathogenesis of knee osteoarthritis (KOA). Thus, this study was conducted to screen the matrisome-associated diagnostic genes for KOA. Results: A total of 158 matrisome-related genes in KOA were obtained, then 5 diagnostic genes were screened, namely collagen type 1 alpha 1 (COL1A1), high temperature requirement factor A1 (HTRA1), SPARC (osteonectin), cwcv and kazal-like domains proteoglycan 1 (SPOCK1), sulfatase 1 (SULF1) and extracellular matrix protein 1 (ECM1). These 5 diagnostic genes were both obviously overexpressed in KOA groups relative to those in the healthy group, and both strongly associated with most immune cells, such as macrophage, eosinophil, and activated B cell. The targeted drugs for the 5 diagnostic genes contained 9-Octadecenamide, Diacerein, and Rifaximin. The mRNA and protein expression levels of the 5 diagnostic genes were consistent with the bioinformatics analysis results. Also, the viability of monosodium iodoacetate (MIA)-treated SW1353 cells was significantly decreased after upregulation of ECM1, while apoptosis showed the opposite trend. Moreover, MIA remarkably increased the phosphorylation levels of PI3K and Akt in SW1353 cells. Conclusions: Five matrisome-associated diagnostic genes were identified with better diagnostic values, including COL1A1, HTRA1, SPOCK1, SULF1 and ECM1. ECM1 exacerbates the progression of KOA, and PI3K-Akt signaling pathway is involved in the progression of KOA. The drugs, containing 9-Octadecenamide, Diacerein, and Rifaximin, etc., might be used for KOA treatment by targeting COL1A1, HTRA1, SPOCK1, SULF1 and ECM1. How to cite: Sun J, Yu G, Zhao Y, et al. Identification and verification of diagnostic biomarkers related to matrisome inpatients with knee osteoarthritis based on machine learning algorithms. Electron J Biotechnol 2026;81. https://doi.org/10.1016/j.ejbt.2026.100710. (c) 2026 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Background The Pseudomonas aeruginosa PAO1 strain is a foundation of research on bacterial virulence and antibiotic resistance. However, its tendency for microevolution during laboratory culture can lead to genetic and phenotypic divergence, potentially compromising experimental reproducibility. This study aimed to systematically characterize such variations in laboratory-maintained MPAO1 sublines to assess their genetic stability and suitability for research. Results We identified two distinct MPAO1 sublines (MPAO1-P and MPAO1-M) with divergent phenotypes. MPAO1-M exhibited markedly increased antimicrobial susceptibility to multiple antibiotics including ciprofloxacin, imipenem, gentamicin and chloramphenicol, while concurrently displaying enhanced production of key virulence factors, including pyocyanin, rhamnolipids, elastase, and twitching motility. Whole-genome resequencing uncovered a novel missense mutation in the mexT gene of MPAO1-M. Consistent with this finding, quantitative reverse transcription PCR analysis revealed a significant downregulation of the mexEF-oprN efflux pump operon and a marked upregulation of the quorum-sensing genes rhlI and pqsA. Conclusions Our findings confirm the critical impact of microevolution on MPAO1 genotype and phenotype, underscoring the necessity of strain verification in experimental design. We further identify a novel mexT mutation as a potential mechanistic driver of these changes, providing new insights into the genetic basis of adaptive evolution in laboratory P. aeruginosa strains.
Background: Resveratrol (RES) has been found to inhibit the progression of lung cancer. Our study aims to explore the molecular mechanisms by which RES regulates lung adenocarcinoma (LUAD) progression. Results: Our study unveils two key novel findings: First, our study demonstrates that EPHB2 is a direct functional target of RES in LUAD. Molecular docking and CETSA confirmed the binding, and crucially, EPHB2 overexpression reversed the anti-tumor effects of RES. Second, our study reveals a previously unrecognized role for EPHB2 in promoting glycolysis in LUAD, which is effectively suppressed by RES. Specifically, RES potently inhibited LUAD tumor growth in vivo and suppressed cell proliferation, migration, invasion, and glycolysis in vitro. These inhibitory effects were consistently abolished upon EPHB2 overexpression. Conclusions: Collectively, our findings suggest that RES inhibits LUAD cell proliferation, migration, invasion, and glycolysis, with EPHB2 downregulation appearing to contribute to these effects. Further studies are needed to determine whether RES directly targets EPHB2 and to evaluate the translational potential of these findings.How to cite: Chen N, Yang Y, Chen Z, et al. Exploring the molecular mechanism of resveratrol for the treatment of lung adenocarcinoma based on molecular docking. Electron J Biotechnol 2026;80. https://doi.org/10.1016/j.ejbt.2026.100706.
Background: Sepsis is a life-threatening condition characterized by organ dysfunction caused by a dysregulated host response to infection. Despite improvements in clinical management, both incidence and mortality remain high. Identifying biomarkers with high sensitivity and specificity is critical for early diagnosis. CD64, an Fcc receptor upregulated on neutrophils during infection, has emerged as a promising diagnostic indicator. This study aimed to evaluate the diagnostic and mechanistic role of CD64 in pediatric sepsis. Results: A total of 200 children with sepsis and 166 healthy controls were enrolled. At a cutoff value of 0.165, the CD64 index achieved a diagnostic sensitivity of 87.0% and specificity of 92.8%, outperforming conventional markers such as procalcitonin (PCT), C-reactive protein (CRP), interleukin-1(3 (IL-1(3), and interleukin-6 (IL-6). Mechanistic assays demonstrated that lipopolysaccharide (LPS) stimulation induced CD64 expression through the Protein Kinase B (AKT) signaling pathway. Both LPS exposure and AKT over-expression promoted p65 nuclear translocation, and chromatin immunoprecipitation confirmed p65 binding to the CD64 promoter, thereby enhancing CD64 transcription. Conclusions: CD64 exhibits superior diagnostic and prognostic performance compared to traditional inflammatory markers and serves as a reliable biomarker for pediatric sepsis. Mechanistically, CD64 upregulation is mediated by the AKT/p65 signaling axis. These findings provide a foundation for integrating CD64 into early diagnostic workflows and developing targeted therapeutic strategies in sepsis management. How to cite: Li L, Fu X, Chen N, et al. AKT/p65-dependent upregulation of CD64 by LPS drives pathogenesis and diagnostic potential in sepsis. Electron J Biotechnol 2026;80. https://doi.org/10.1016/j.ejbt.2026. 100707. (c) 2026 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Background: Head and neck cancer (HNC) is one of the most prevalent and challenging diseases affecting a large population worldwide. Functional genomics can help understand the disease, but expressed gene therapy is uncertain. The study sought to identify specific genetic mutations and protein expression profiles in HNC. Results: We ranked IFNG, SULF1, and OAS3 as three HNC-related genes (p < 0.05) based on the data mining. N-acetyleglucosamine-6-sulfatase activity, arylsulfatase, 2,5-oligoadenylate synthetase activity, interferon-gamma receptor binding, and other essential biological processes were all significantly correlated with the gene ontology (GO) terms. Nucleotide excision repair pathways, RNA polymerase-I transcription start and termination, RNA polymerase-II promoter escape, pyrimidine biosynthesis, and interferon-gamma signaling were all linked in the pathway enrichment. OAS1, IFIT1, CD4, STAT3, NFKBIA, RIPK1, SLCO5A1, and others are functionally connected to the co-expressed genes, while COL3A1 and SCEL are indirectly linked. Compared to controls, the quantitative PCR (qPCR) of these genes showed a significant two-fold change (FC) expression (2-DDC T ) pattern of SULF1 (FC <= 1.2), OAS3 (FC <= 0.13), and IFNG (FC <= 0.12) compared to reference gene GAPDH (FC = 1). Pathophysiological cancer development is associated with up-and downregulated expression of these genes. The study found that personalized medicine can improve HNC treatment by adapting medication to each patient's tumor's molecular traits. Conclusions: A substantial correlation between the pathophysiology of HNC and the IFNG, SULF1, and OAS3 genes is found. This research could expedite the progress of drug discovery and aid in modifying HNC's treatment approaches. How to cite: Khawar J, Guo J, Akhtar S, et al. Systems-level analysis prioritizes the importance of IFNG, SULF1, and OAS3 genes in head and neck cancer. Electron J Biotechnol 2026;80. https://doi.org/10. 1016/j.ejbt.2026.100705. (c) 2026 The Authors. Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/ by-nc-nd/4.0/).
Background: Doxorubicin (DOX), a widely used chemotherapeutic agent, causes severe cardiotoxicity that frequently progresses to dilated cardiomyopathy (DCM). While ankyrin repeat domain 1 protein (ANKRD1) plays critical roles in cardiovascular pathophysiology, its specific involvement in doxorubicin-induced DCM remains unknown. This study investigates the functional significance of ANKRD1 in DOX-induced DCM pathogenesis. Results: DOX treatment significantly upregulated ANKRD1 expression in both rat models and H9c2 rat cardiomyocytes. In vivo, ANKRD1 knockdown ameliorated DOX-induced cardiac dysfunction, as demonstrated by improved left ventricular ejection fraction and fractional shortening, along with reduced serum levels of lactate dehydrogenase and creatine kinase-myocardial band. Conversely, ANKRD1 overexpression exacerbated cardiac impairment. Pathological examination revealed that ANKRD1 knockdown attenuated DOX-induced myocardial tissue damage and collagen deposition, while ANKRD1 overexpression intensified these pathological changes. Furthermore, ANKRD1 knockdown mitigated mitochondrial dysfunction and oxidative stress in DCM models both in vivo and in vitro. Mechanistically, ANKRD1 knockdown activated the AMP-activated protein kinase (AMPK)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling cascade, thereby attenuating DOX-induced cardiomyocyte toxicity, mitochondrial dysfunction, and oxidative stress. Rescue experiments using the AMPK inhibitor dorsomorphin confirmed this pathway's involvement, as dorsomorphin treatment abolished the protective effects of ANKRD1 knockdown against DOX-induced cardiomyocyte damage. Conclusions: ANKRD1 knockdown prevents DOX-induced DCM by ameliorating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. These findings establish ANKRD1 as a promising therapeutic target for preventing DOX-induced cardiotoxicity and DCM.
Background: Actinomycetes are gram-positive bacteria that belong to the actinobacterial species. They are a prolific source of secondary metabolites with various biological applications. Thus, this study aimed to culture-based isolation of potent Actinomycete species from Sof-Umer Cave and in vitro and in vivo evaluation of their potential metabolites against selected test organisms. Result: Among the total isolates, ten isolates were selected based on their antimicrobial activities. Among them, the ethyl acetate crude extract of three isolates (RO13, SD2, R011) showed potential antagonistic activity, ranging from 17 +/- 0.78 to 23 +/- 0.56 mm of zone of inhibition against Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus. Additionally, two isolates' (SD2, R011) crude extract exhibited significant inhibition of test organisms in wound and oral infection of the mice models. This was confirmed by wound contraction and progress improvement of the clinical sign observed before treatment. Characterization of their crude extract by FTIR and GC-MS revealed the presence of various functional groups and compounds. Specifically, potent antimicrobial and antioxidant bioactive compounds, such as pyrrolo[1,2-a]pyrazine-1,4-dione, hexahydro-2-piperidine, phenol, 2-methoxy-4-(1-propenyl)-, and indolizine, were identified via GC-MS analysis. Three of the ten potent isolates (R013, R011, and SD2) were identified based on the 16S rRNA gene sequence, and the R013 isolate belongs to Streptomycetes flavoviridis, whereas SD2 and R011 were identified as Arthrobacter sp. and Actinobacterium kmd_152, respectively. Conclusions: Sof-Umer cave-dwelling actinomycetes possess potent metabolites against test organisms that can be a base for future potent drug development against microbial infections. How to cite: Abdeta EC, Meka AF, Hordofa DG, et al. Metabolites of native actinomycetes from Sof Umer cave reveal potent antimicrobial activity against selected pathogens in mice infection models. Electron J Biotechnol 2026;79. https://doi.org/10.1016/j.ejbt.2025.100703. (c) 2025 The Author(s). Published by Elsevier Inc. on behalf of Pontificia Universidad Cat oe lica de Valpara & Uacute;so. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
