Biology subjects

Zheng, L.

Publications and source records attributed to Zheng, L..

At least 73 records · Page 4Linked to original sources

bioRxiv2025

Brain Diffusion Transformer for Personalized Neuroscience and Psychiatry

Task-fMRI analyses typically focus on localized activation contrasts between stimuli, neglecting the brains dynamic hierarchy. We introduce Brain Diffusion Transformer (Brain-DiT), a deep generative model capturing recurrent processing underlying individualized neurocognitive state transitions via functional networks. Without prior assumptions, Brain-DiT identifies canonical cognitive regions in the brain and reveals replicable subgroups with distinct neural circuits in large cohorts, offering critical clinical insights overlooked by traditional methods: individuals exhibiting negative emotion bias, linked to language-related regions, had a 12-fold higher likelihood of major depression, and those with maladaptive inhibition strategies, associated with overactive medial frontal regions, showed a 9-fold increased risk of alcohol abuse. By bridging cognitive theory and psychiatric applications, Brain-DiT provides a unified analytical paradigm, paving the way for operational personalized medicine in psychiatry.

neuroscience↗

bioRxiv2025

DNA2 and MSH2 activity collectively mediate chemically stabilized G4 for efficient telomere replication

G-quadruplexes (G4s) are widely existing stable DNA secondary structures in mammalian cells. A long-standing hypothesis is that timely resolution of G4s is needed for efficient and faithful DNA replication. In vitro, G4s may be unwound by helicases or alternatively resolved via DNA2 nuclease mediated G4 cleavage. However, little is known about the biological significance and regulatory mechanism of the DNA2-mediated G4 removal pathway. Here, we report that DNA2 deficiency or its chemical inhibition leads to a significant accumulation of G4s and stalled replication forks at telomeres, which is demonstrated by a high-resolution technology: Single molecular analysis of replicating DNA (SMARD). We further identify that the DNA repair complex MutS (MSH2-MSH6) binds G4s and stimulates G4 resolution via DNA2-mediated G4 excision. MSH2 deficiency, like DNA2 deficiency or inhibition, causes G4 accumulation and defective telomere replication. Meanwhile, G4-stabilizing environmental compounds block G4 unwinding by helicases but not G4 cleavage by DNA2. Consequently, G4 stabilizers impair telomere replication and cause telomere instabilities, especially in cells deficient in DNA2 or MSH2.

molecular biology↗

bioRxiv2025

The Immune-Modulatory Function of Megakaryocytes in the Hematopoietic Niche of Myeloproliferative Neoplasms

Myeloproliferative neoplasms (MPNs) are clonal stem cell disorders characterized by dysregulated megakaryopoiesis and neoplastic hematopoietic stem cell (HSC) expansion. Using a murine model with MK-specific JAK2V617F expression, we establish an MPN aging model where mutant MKs drive HSC expansion and a progressive decline in wild-type HSC function. Compared to wild-type MKs, JAK2V617F MKs exhibit heightened inflammation and innate immune activation with aging, including increased antigen presentation, elevated pro-inflammatory cytokines, skewed T cell populations, and impaired T cell functions in the marrow niche. Enhanced MK immunomodulatory function is linked to mutant cell expansion and MPN progression in a chimeric murine model with co-existing wild-type and JAK2V617F mutant HSCs. LINE-1 (long-interspersed element-1), a retrotransposon linked to innate immune activation and aging, is upregulated in mutant MKs during aging in murine models. We validated that LINE-1-encoded protein ORF1p is expressed in marrow MKs in 12 of 13 MPN patients but absent in control samples from patients undergoing orthopedic surgery (n=5). These findings suggest that MKs reprogram the marrow immune microenvironment, impairing normal HSC function while promoting neoplastic expansion in MPNs. LINE-1 activation in mutant MKs may be a key driver of immune dysregulation in MPNs. Key PointsO_LIJAK2V617F mutant MKs reprogram the marrow immune microenvironment to promote neoplastic HSC expansion in MPNs. C_LIO_LILINE-1 activation in diseased MKs triggers chronic inflammation and immune dysfunction in MPNs. C_LI

cancer biology↗

bioRxiv2025

Volumetric 3D Printing and Melt-Electrowriting to Fabricate Implantable Reinforced Cardiac Tissue Patches

Cardiac patches for repairing myocardial defects require mechanically stable materials that prevent bleeding and can be implanted via suturing. The current clinical standard, bovine pericardial patches (BPPs), serve this purpose but do not degrade or integrate with the myocardium, limiting their long-term effectiveness. Therefore, we have developed the Reinforced engineered Cardiac tissue Patch (RCPatch). This multimaterial patch consists of a stiffness-tuned, cardiomyocyte-infiltrated 3D metamaterial and a suturable, hydrogel-infiltrated mesh to reduce permeability and bleeding. We first designed and computationally optimized anisotropic metamaterials using a generative modelling approach and fabricated them from biodegradable poly({varepsilon}-caprolactone) (PCL) via volumetric 3D printing (VP). The metamaterial supported the infiltration of cardiomyocytes, which maintained cell viability and contractility in vitro. In a second step, we enhanced implantability and reduced blood permeability through the patch by combining a melt-electrowritten (MEW) mesh with a fibrin hydrogel. Finally, in an acute large animal trial, the RCPatch was used on an induced myocardial defect, where it withstood intraventricular blood pressure and enabled partial hemodynamic recovery. Our findings establish a scalable framework for fabricating cardiac tissue patches that integrate mechanical reinforcement with biological function, offering a surgically implantable, and potentially regenerative solution for intraventricular myocardial repair. Table of Contents (ToC) O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=179 SRC="FIGDIR/small/642643v1_ufig1.gif" ALT="Figure 1"> View larger version (64K): org.highwire.dtl.DTLVardef@66293dorg.highwire.dtl.DTLVardef@11d9122org.highwire.dtl.DTLVardef@235d16org.highwire.dtl.DTLVardef@1b46911_HPS_FORMAT_FIGEXP M_FIG C_FIG This study presents an implantable intraventricular cardiac patch (RCPatch) combining volumetric 3D-printed metamaterials with melt-electrowritten (MEW) meshes. The design integrates tunable stiff structures with soft, cell-laden hydrogels. The RCPatch withstood suturing, intraventricular pressure, and cardiac contraction in an acute large animal myocardial defect model. The patch prevented bleeding and enabled partial hemodynamic recovery, demonstrating its potential for myocardial repair.

bioengineering↗

bioRxiv2025

Benchmarking AlphaFold3-like Methods for Protein-Peptide Complex Prediction

Protein-short peptide interactions are central mechanisms regulating signal transduction, chaperone functions, and drug targeting design. However, the precise prediction of their complex structures has long been constrained by the limited accuracy of traditional methods. The breakthrough of AlphaFold2 resolved the challenge of predicting protein monomer structures. Its derivative method, AlphaFold2-multimer, surpassed traditional docking approaches in predicting protein complexes, yet its accuracy remains suboptimal. AlphaFold3 and its replication models, such as Protenix, Chai-1, and Boltz-1, have further improved prediction accuracy for protein-protein interactions. To evaluate the performance of these methods in protein-short peptide structure prediction, this study conducted predictions and comprehensive comparisons on two benchmark datasets of protein-short peptide complexes. One dataset did not intentionally exclude structures from the training set of these methods, while the other did. For the former, the results demonstrate that the new-generation structural method significantly increased the success rate under stringent criteria (Fnat[≥] 0.8) to 70-80%, compared to AlphaFold2-multimer (53%), with Protenix achieving the highest accuracy at 80.8%. For the second dataset, AlphaFold2-multimer showed consistent performance, but the success rates of the new-generation methods all dropped significantly (to 40-56%). Our analysis suggests that the main challenge for the performance decline comes from the accurate prediction of binding sites. For all datasets, A multi-method combination strategy enabled a higher-quality prediction success rate compared to the individual models, highlighting synergistic advantages among methods. Notably, inter-model consistency analysis provided an efficient metric for selecting optimal predictions.

bioinformatics↗

bioRxiv2025

Endurance Exercise Ameliorates Aging-Related Bradyarrhythmia in Drosophila Resulting from miR-283 Knockdown in LNvs

MicroRNAs (miRNAs) are crucial in regulating cardiac aging and related diseases, yet few functional miRNAs have been identified. Prior studies showed miR-216a upregulation in heart failure patients, but its impact on aging hearts is unknown. Our study revealed systemic miR-283 overexpression or knockdown caused age-related bradycardia, mimicking human bradyarrhythmia. Importantly, we found that knockdown of miR-283 in ventral-lateral neurons (LNvs), rather than in the heart, led to the occurrence of bradyarrhythmia, which was mainly caused by the upregulation of miR-283 expression in the whole brain and heart. The gene of clockwork orange (cwo) may mediate miR-283s effect on heart rhythm. Additionally, to investigate the miRNA regulatory mechanism underlying exercise-induced delay in cardiac aging, we conducted a three-week endurance exercise program on miR-283 knockdown flies in LNvs. We found that exercise significantly downregulated the accumulation of miR-283 in the brain and myocardium caused by aging or miR-283 knockdown in LNvs, improved the structure of myocardial fibers, and effectively reduced bradyarrhythmia. Our findings provides a new perspective on distal neuromodulation and intervention in cardiac aging.

physiology↗

bioRxiv2025

Highly accurate prophage island detection with PIDE

As important mobile elements in prokaryotes, prophages shape the genomic context of their hosts and regulate the structure of bacterial populations. However, it is challenging to precisely identify prophages through computational methods. Here, we introduce PIDE for identifying prophages from bacterial genomes or metagenome-assembled genomes. PIDE integrates a pre-trained protein language model and gene density clustering algorithm to distinguish prophages. Benchmarking on bacterial genomes with experimental prophage annotation demonstrates that PIDE pinpoints prophages with precise boundaries. Applying PIDE to 4,744 human gut representative genomes reveals 24,467 prophages with widespread functional capacity. PIDE is open source and is available at https://github.com/chyghy/PIDE.

bioinformatics↗

bioRxiv2025

Fibroblast growth factor 21 regulates neuromuscular junctioninnervation through HDAC4 in denervation-induced skeletal muscle atrophy

Skeletal muscles undergo atrophy in response to denervation and neuromuscular diseases. Understanding the mechanisms by which denervation drives muscle atrophy is crucial for developing therapies against neurogenic muscle atrophy. Here, we identify muscle-secreted fibroblast growth factor 21 (FGF21) as a key inducer of atrophy following muscle denervation. In denervated skeletal muscles, FGF21 is uniquely upregulated among the FGF family members and acts in an autocrine/paracrine manner to promote muscle atrophy. Silencing FGF21 in muscle prevents denervation-induced muscle wasting by preserving neuromuscular junction (NMJ) innervation. Conversely, forced expression of FGF21 in muscle reduces NMJ innervation, leading to muscle atrophy. Mechanistically, TGFB1 released by denervated fibro-adipogenic progenitors (FAPs) upregulates FGF21 through the JNK/c-Jun axis, which in turn reduces the cytoplasmic level of histone deacetylase 4 (HDAC4), culminating in muscle atrophy. HDAC4 knockdown abolishes the atrophy-resistant effects observed in FGF21-deficient denervated muscles, resulting in muscle atrophy. Our findings reveal a novel role and heretofore unrecognized mechanism of FGF21 in skeletal muscle atrophy, suggesting that inhibiting muscular FGF21 could be a promising strategy for mitigating skeletal muscle atrophy.

biochemistry↗

bioRxiv2025

Direct Optical Detection of Factor Xa Activity in Minimally Processed Whole Blood

The ability to measure factor Xa activity directly in whole blood samples offers a path toward point-of-care monitoring and personalized anticoagulant dosage, potentially reducing bleeding risk and other anticoagulant-associated complications. We present a strategy to enable direct optical detection of factor Xa in minimally processed whole blood samples. Our strategy relies on a custom FRET-pair labeled DNA-peptide substrate, allowing FRET ratio to be monitored as an indicator of factor Xa activity. Substrates are tethered to a tapered-fiber sensor to allow evanescent detection of fluorescence directly at the sensor surface, minimizing background media interference and enabling detection directly in blood samples. After characterizing the custom substrate and demonstrating the correlation of fiber-based measurements to an existing chromogenic assay, we demonstrate the detection of endogenous factor Xa activity in >85% whole blood. Finally, we demonstrate the detection of therapeutic concentrations of enoxaparin, a widely used anticoagulant, directly in 90% whole blood in less than an hour and correlate these measurements to activated partial thromboplastin time (aPTT) testing. Together, these results indicate a promising strategy to achieve point-of-care factor Xa detection, enabling personalized anticoagulant treatment and reducing adverse outcomes.

bioengineering↗

bioRxiv2025

Cancer associated fibroblasts drive epithelial to mesenchymal transition and classical to basal change in pancreatic ductal adenocarcinoma cells with loss of IL-8 expression

Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, in part resulting from cellular heterogeneity that supports overall tumorigenicity. Cancer associated fibroblasts (CAF) are key determinants of PDAC biology and response to systemic therapy. While CAF subtypes have been defined, the effects of patient-specific CAF heterogeneity and plasticity on tumor cell behavior remain unclear. Here, multi-omics was used to characterize the tumor microenvironment (TME) in tumors from patients undergoing curative-intent surgery for PDAC. In these same patients, matched tumor organoid and CAF lines were established to functionally validate the impact of CAFs on the tumor cells. CAFs were found to drive epithelial-mesenchymal transition (EMT) and a switch in tumor cell classificiaton from classical to basal subtype. Furthermore, we identified CAF-specific interleukin 8 (IL-8) as an important modulator of tumor cell subtype. Finally, we defined neighborhood relationships between tumor cell and T cell subsets. Statement of SignificanceThis multidimensional analysis highlights the diverse role CAFs have in influencing other cell types in the TME, including epithelial-derived tumor and infiltrating immune cells. Our methods provide a platform for evaluating emerging therapeutic approaches and for studying mechanisms that dictate tumor behavior in a manner that reflects patient-specific heterogeneity.

cancer biology↗

bioRxiv2025

Pathobiont-triggered induction of epithelial IDO1 drives regional susceptibility to Inflammatory Bowel Disease

The structure and function of the mammalian gut vary by region, yet why inflammatory diseases manifest in specific regions and not others remains unclear. We use a TNF-overexpressing Crohns disease (CD) model (Tnf{Delta}ARE/+), which typically presents in the terminal ileum (TI), to investigate how environmental factors interact with the hosts immune susceptibility to drive region-specific disease. We identified Chlamydia muridarum, an intracellular bacterium and murine counterpart to the human sexually transmitted C. trachomatis, as necessary and sufficient to trigger disease manifestation in the ascending colon (AC), another common site of human CD. Disease manifestation in the AC depends on indoleamine 2,3-dioxygenase (IDO1) activity induced by hypersensitive surface secretory cells in genetically susceptible hosts. Single-cell and microbial analyses of human specimens also implicates this pathobiont-epithelial IDO1 pathway in patients with a history of CD in the AC. Our findings demonstrate that genetic and microbial factors can independently drive region-specific disease and provide a unique model to study CD specific to the AC.

cell biology↗

bioRxiv2025

Phosphorus Availability Modulates Flowering Time Through Subcellular Reprogramming of bGLU25 and GRP7 in Flowering Plants

The transition from vegetative to reproductive growth is vital for plant fitness and crop yield and is strongly influenced by nutrient availability. While nitrogen deficiency accelerates flowering, phosphorus (P) limitation delays it. However, the molecular basis for how P availability regulates flowering time remains unclear. Here, through genome-wide association mapping in Arabidopsis, we uncover genetic variation in {beta}-GLUCOSIDASE 25 (bGLU25) that modulates flowering under P-limited conditions. In P-sufficient environments, bGLU25 localizes to the endoplasmic reticulum. Under P limitation, however, bGLU25 translocates to the cytosol, a process mediated by P-regulated SERINE CARBOXY PEPTIDASE 50 (SCP50). In the cytosol, bGLU25 binds to JACALIN-LECTIN LIKE1 (AtJAC1), preventing the nuclear translocation of the Flowering Locus C (FLC) regulator GLYCINE-RICH RNA-BINDING PROTEIN 7 (GRP7). This cytosolic sequestration of GRP7 under P-deprivation elevates FLC expression, delaying flowering. Moreover, in the monocot rice, the homologs of bGLU25 also modulate flowering responses to P availability, indicating a conserved role for bGLU25 across flowering plants. Our findings provide a molecular framework for breeding strategies aimed at optimizing flowering time in response to P levels.

plant biology↗

bioRxiv2024

Deciphering the thiolactonization mechanism in thiolactomycin biosynthesis

Thiolactomycin (1), which features a unique{gamma} -thiolactone ring, is a promising antibiotic candidate that specifically targets bacterial type II fatty acid synthase. Despite extensive studies on its pharmacological activities, modes of action, and chemical synthesis, the enzymatic processes responsible for forming the activity-determining{gamma} -thiolactone ring have remained largely unknown. Here, we resolve this problem by revealing that the condensation and heterocyclization (Cy) domain of the nonribosomal peptide synthetase (NRPS) TlnC (TlnCCy), along with the cytochrome P450 enzyme TlnA, cooperatively enable the{gamma} -thiolactone assembly. TlnCCy mediates an unusual sulfurtransfer reaction to sulfurate the polyketide intermediate, generating a thiocarboxylate intermediate. Subsequently, TlnA acts as a{gamma} -thiolactone synthase, converting the linear thiocarboxylate intermediate into 1 via a distal radical-based cyclization mechanism. These findings not only expand the functional and catalytic repertoires of NRPS Cy domains and P450 enzymes, but also highlight a special enzymatic strategy for{gamma} -thiolactone biosynthesis in nature. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/629141v2_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@7e0ad2org.highwire.dtl.DTLVardef@f86b80org.highwire.dtl.DTLVardef@159d136org.highwire.dtl.DTLVardef@1b633ff_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2024

GlioME: A Novel Organoid Model Retaining the Glioma Mi-croenvironment for Personalized Drug Screening and Thera-peutic Evaluation

Glioma is an aggressive brain tumor with a poor prognosis. Establishing an in vitro culture model that closely replicates the cellular composition and microenvironment of the original tumor has been challenging, limiting its clinical applications. Here, we present a novel approach to generate glioma organoids with a microenvironment (GlioME) from patient-derived glioma tissue. These organoids maintain the genetic and epigenetic characteristics of the primary tumor and preserve cell-to-cell interactions within the tumor microenvironment, including resident immune cells. Bulk RNA sequencing, whole exome sequencing, and DNA methylation analysis were used to confirm the molecular similarities between the organoids and primary glioma tissues. Immunofluorescence and flow cytometry were used to assess immune cell viability, comparing GlioME with floating glioma organoids. GlioME exhibited high responsiveness to chemotherapy and targeted therapy, demonstrating its potential for therapeutic screening applications. Notably, GlioME accurately predicted patient response to the recently approved MET inhibitor, vebreltinib. Thus, this organoid model provides a reliable in vitro platform for glioma microenvironment-related research and clinical drug screening.

cancer biology↗

bioRxiv2024

Mapping cell-cell fusion at single-cell resolution

Cell-cell fusion is a tightly controlled process in the human body known to be involved in fertilization, placental development, muscle growth, bone remodeling, and viral response. Fusion between cancer cells results first in a whole-genome doubled state, which may be followed by the generation of aneuploidies; these genomic alterations are known drivers of tumor evolution. The role of cell-cell fusion in cancer progression and treatment response has been understudied due to limited experimental systems for tracking and analyzing individual fusion events. To meet this need, we developed a molecular toolkit to map the origins and outcomes of individual cell fusion events within a tumor cell population. This platform, ClonMapper Duo ( CMDuo), identifies cells that have undergone cell-cell fusion through a combination of reporter expression and engineered fluorescence-associated index sequences paired to randomly generated nucleotide barcodes. scRNA-seq of the indexed barcodes enables the mapping of each set of parental cells and fusion progeny throughout the cell population. In triple-negative breast cancer cells CMDuo uncovered subclonal transcriptomic hybridization and unveiled distinct cell-states which arise in direct consequence of homotypic cell-cell fusion. CMDuo is a platform that enables mapping of cell-cell fusion events in high-throughput single cell data and enables the study of cell fusion in disease progression and therapeutic response.

systems biology↗

bioRxiv2024

Reconstitution of SPO11-dependent double-strand break formation

Homologous meiotic recombination starts with DNA double-strand breaks (DSBs) generated by SPO11 protein1. SPO11 is critical for meiosis in most species but the DSBs it makes are also dangerous because of their mutagenic2 and gametocidal3 potential, so cells must foster SPO11s beneficial functions while minimizing its risks4. SPO11 mechanism and regulation remain poorly understood. Here we report reconstitution of DNA cleavage in vitro with purified recombinant mouse SPO11 bound to its essential partner TOP6BL. Similar to their yeast orthologs5,6, SPO11- TOP6BL complexes are monomeric (1:1) in solution and bind tightly to DNA. Unlike in yeast, however, dimeric (2:2) assemblies of mouse SPO11-TOP6BL cleave DNA to form covalent 5' attachments requiring SPO11 active site residues, divalent metal ions, and SPO11 dimerization. Surprisingly, SPO11 can also manifest topoisomerase activity by relaxing supercoils and resealing DNA that it has nicked. Structure modeling with AlphaFold37 illuminates the protein-DNA interface and suggests that DNA is bent prior to cleavage. Deep sequencing of in vitro cleavage products reveals a rotationally symmetric base composition bias that partially explains DSB site preferences in vivo. Cleavage is inefficient on complex DNA substrates, partly because SPO11 is readily trapped in DSB-incompetent (presumably monomeric) binding states that exchange slowly. However, cleavage is improved by using substrates that favor DSB-competent dimer assembly, or by fusing SPO11 to an artificial dimerization module. Our results inform a model in which intrinsically feeble dimerization restrains SPO11 activity in vivo, making it exquisitely dependent on accessory proteins that focus and control DSB formation so that it happens only at the right time and the right places.

biochemistry↗

bioRxiv2024

Harnessing Protein Language Model for Structure-Based Discovery of Highly Efficient and Robust PET Hydrolases

Plastic waste, particularly polyethylene terephthalate (PET), presents significant environmental challenges, prompting extensive research into enzymatic biodegradation. Existing PET hydrolases are limited to a narrow sequence space and demonstrate insufficient performance for biodegradation. This study introduces a novel discovery pipeline that combines protein language models (PLMs) with a structural representation tree to identify enzymes based on structural similarity. Using the crystal structure of IsPETase as a template, we employed PLMs and a representation tree to efficiently search and cluster target proteins. Screening of candidate proteins was further refined using PLM-based assessments of solubility and thermal stability. Biochemical experiments showed that 14 of 34 candidates exhibited PET degradation activity across a temperature range of 30-60 {degrees}C. Notably, we identified a PET hydrolase -KbPETase, which possesses a melting temperature 32 {degrees}C higher than that of IsPETase and exhibits the highest PET degradation activity within 30-50 {degrees}C compared to other wild-type PETases. KbPETase also shows higher catalytic efficiency than FastPETase. X-ray crystallography and molecular dynamics simulations further revealed that KbPETase has a conserved catalytic domain and enhanced intramolecular interactions. This work develops a novel deep learning approach to discover natural PETases with enhanced functions.

molecular biology↗

bioRxiv2024

PMAIP1-Mediated Glucose Metabolism and its Impact on the Tumor Microenvironment in Breast Cancer: Integration of Multi-Omics Analysis and Experimental Validation

BackgroundGlucose metabolism in breast cancer has a potential effect on tumor progression and is related to the immune microenvironment. Thus, this study aimed to develop a glucose metabolism- tumor microenvironment score to provide new perspectives on breast cancer treatment. MethodData were acquired from the Gene Expression Omnibus and UCSC Xena databases, and glucose-metabolism-related genes were acquired from the Gene Set Enrichment Analysis database. Genes with significant prognostic value were identified, and immune infiltration analysis was conducted, and a prognostic model was constructed based on the results of these analyses. The results were validated by in vitro experiments with MCF-7 and MCF-10A cell lines, including expression validation, functional experiments, and bulk sequencing. Single-cell analysis was also conducted to explore the role of specific cell clusters in breast cancer, and Bayes deconvolution was used to further investigate the associations between cell clusters and tumor phenotypes of breast cancer. ResultsFour significant prognostic genes (PMAIP1, PGK1, SIRT7, and SORBS1) were identified, and, through immune infiltration analysis, a combined prognostic model based on glucose metabolism and immune infiltration was established. The model was used to classify clinical subtypes of breast cancer, and PMAIP1 was identified as a potential critical gene related to glucose metabolism in breast cancer. Single-cell analysis and Bayes deconvolution jointly confirmed the protective role of the PMAIP1+ luminal cell cluster.

bioinformatics↗