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EMCN is associated with vascular-immune crosstalk and represents a potential biomarker in lung adenocarcinoma
Front Mol Biosci. 2026 Aug 12;13:1752442. doi: 10.3389/fmolb.2026.1752442. eCollection 2026.
ABSTRACT
BACKGROUND: While MUC family genes have been established as prognostic biomarkers in gastric cancer, and GWAS studies link EMCN mutations to chemotherapy-induced myelosuppression in NSCLC, the systematic characterization of EMCN in lung adenocarcinoma (LUAD) remains elusive.
METHODS: This multi-omics strategy combining bulk and single-cell transcriptomics study integrated differential expression analysis, WGCNA, and machine learning algorithms (LASSO/SVM-RFE/Random Forest) to identify EMCN as a diagnostic hub gene, followed by experimental validation using immunohistochemistry Western blot and qRT-PCR.
RESULTS: EMCN (Endomucin) is a sialomucin-like glycoprotein predominantly expressed in vascular endothelial cells. Using bulk transcriptomic datasets and single-cell RNA-seq analysis, we found that EMCN expression was reduced in lung adenocarcinoma (LUAD) compared with non-tumor controls and was primarily localized to the endothelial compartment. Survival analysis using the median expression cutoff showed that high EMCN expression was associated with improved overall survival (Cox HR_high vs. low = 0.73, p = 0.04), indicating that low EMCN expression correlates with poorer prognosis. Machine learning-based feature selection (LASSO, Random Forest, and SVM) further prioritized EMCN among consensus candidate genes, supporting its potential relevance to the vascular-associated tumor microenvironment in LUAD. EMCN expression levels also showed a significant positive correlation with the degree of immune cell infiltration. Gene set enrichment analysis (GSEA) revealed that high EMCN expression in tumor tissues activates negative regulatory pathways associated with angiogenesis. Receiver operating characteristic (ROC) curve analysis highlights EMCN's excellent diagnostic potential for LUAD, with an area under the curve (AUC) of 0.963. In vitro experiments confirm the downregulation of EMCN at both protein and mRNA levels, consistent with our bioinformatics predictions.
CONCLUSION: This first comprehensive study establishes EMCN as a dual-functional regulator of vascular-immune crosstalk in LUAD, providing both a molecular diagnostic tool and therapeutic target for precision oncology.
PMID:42656419 | PMC:PMC13506425 | DOI:10.3389/fmolb.2026.1752442
Disruption of the AR/ZNF217/PROM2 axis sensitizes prostate cancer to ferroptosis and enzalutamide therapy
Oncogenesis, Published online: 11 August 2026; doi:10.1038/s41389-026-00649-7
Disruption of the AR/ZNF217/PROM2 axis sensitizes prostate cancer to ferroptosis and enzalutamide therapyActivation of methionine metabolism mediated by HNF4α confers ferroptosis resistance in hepatocellular carcinoma
Cell Death Discovery, Published online: 26 May 2026; doi:10.1038/s41420-026-03165-0
Activation of methionine metabolism mediated by HNF4α confers ferroptosis resistance in hepatocellular carcinomaHigh-fidelity identification of guest species in porous materials
Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10527-2
A reconstruction method based on Gaussian-apodized single-sideband electron ptychography removes artefacts to enable the high-fidelity identification of guest species in porous materials.ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming
Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.
ABSTRACT
Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3β phosphorylation. Combined with ANP32E-mediated GSK3β suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-β-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3β inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.
PMID:41980942 | DOI:10.1038/s41419-026-08712-2
GUIDE: Interpretable GUI Agent Evaluation via Hierarchical Diagnosis
HoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstruction
npj Digital Medicine, Published online: 04 April 2026; doi:10.1038/s41746-026-02573-x
HoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstructionCell-type-specific transposon demethylation and TAD remodeling in aging mouse brain
Gut-Brain Axis Dysregulation in Inflammatory Bowel Disease: Implications for Coagulation Abnormalities and Extraintestinal Manifestations
Int J Gen Med. 2026 Mar 24;19:590621. doi: 10.2147/IJGM.S590621. eCollection 2026.
ABSTRACT
Inflammatory bowel disease (IBD) involves chronic intestinal inflammation driven by gut-brain axis imbalance, fostering complications through an "inflammation-neuro-coagulation" triad. Current staging systems inadequately capture the dynamics of this multidimensional network. Therefore, integrated multi-omics analyses-including metagenomics, metabolomics, and single-cell transcriptomics-are essential to construct dynamic models that monitor coagulation, microbiome, and metabolism for precise assessment of disease activity and thrombotic or bleeding risks. Interventions targeting gut-brain axis nodes, such as eliminating tissue factor-positive (TF⁺) T cells or modulating vagal activity, show potential to disrupt the inflammation-coagulation cycle, although rigorous randomized trials are still needed. Artificial intelligence (AI)-assisted systems that integrate real-time biomarker monitoring with multi-omics predictions represent a novel paradigm for managing IBD-related coagulation dysfunction. Key challenges include elucidating gut-brain-liver axis regulation of coagulation and characterizing platelet functional heterogeneity. Future efforts must prioritize ethically compliant multi-omics platforms and racially stratified risk models to advance personalized coagulation management in IBD.
PMID:41913906 | PMC:PMC13033200 | DOI:10.2147/IJGM.S590621
A multiomics Mendelian randomization study on PANoptosis-related genes and gastric cancer risk
J Int Med Res. 2026 Mar;54(3):3000605261430163. doi: 10.1177/03000605261430163. Epub 2026 Mar 16.
ABSTRACT
ObjectiveTo explore the potential involvement of PANoptosis-related genes in gastric cancer susceptibility through multiomics analyses.MethodsSummary-data-based Mendelian randomization was performed by integrating blood-derived methylation, gene expression, and protein quantitative trait loci data with genome-wide association study results. The findings were further evaluated in The Cancer Genome Atlas cohort, followed by protein-protein interaction analysis, drug prediction, and molecular docking.ResultsSummary-data-based Mendelian randomization and colocalization analyses identified several traits suggestively associated with gastric cancer risk. Genetically predicted higher expression of apoptosis and caspase activation inhibitor (AVEN) and hepatocyte growth factor (HGF) as well as higher HGF protein levels were associated with increased risk, whereas higher levels of protein phosphatase 2 regulatory subunit B beta (PPP2R2B) appeared to be protective. Multiomics integration suggested epigenetic regulation of HGF and PPP2R2B. The Cancer Genome Atlas analysis corroborated the dysregulation of these candidates, with high AVEN expression associated with poorer survival. Protein-protein interaction and drug prediction analyses highlighted functional networks and potential therapeutics, supported by molecular docking demonstrating strong HGF-binding affinities. However, these associations did not reach statistical significance in the independent validation cohort, possibly due to limited statistical power.ConclusionsThis study identified AVEN, HGF, and PPP2R2B as potential candidate genes for gastric cancer. These findings require further validation in larger cohorts.
PMID:41840829 | DOI:10.1177/03000605261430163