About

Hui Li is a Professor of Pathology at the University of Virginia School of Medicine. He holds a BS in Chemical Physics from the University of Science and Technology of China and a PhD in Molecular Biology from Case Western Reserve University. He completed postdoctoral training in Molecular Biology at Yale University. His research disciplines include Biochemistry, Bioinformatics and Genomics, Biotechnology, Cancer Biology, Computational Biology, Development and Stem Cells & Regeneration, Epigenetics, Experimental Pathology, Genetics, Molecular and Cellular Physiology, Molecular Biology, Molecular Physiology and Biological Physics, Neuroscience, Structural Biology, and Translational Science. Professor Li's research focuses on gene regulation in cancer, RNA processing, epigenetic modification, and stem cell and development. His laboratory has identified a novel oncogene that multiple cancers are addicted to, including glioblastoma and pediatric sarcoma, and works on understanding its mechanisms, activation, and developing small molecule inhibitors. His team constructs various animal models to study the biology of this oncogene and test therapeutic compounds. Additionally, his research explores chimeric RNA and system biology, challenging traditional views of gene interaction and revealing mechanisms such as RNA trans-splicing and cis-Splicing of Adjacent Genes (cis-SAGe). These processes generate fusion products without DNA rearrangement, expanding the understanding of gene products in normal physiology and cancer. His long-term goals include elucidating the scope and functions of these phenomena and their implications in development and cancer. He employs a range of approaches from bioinformatics to CRISPR/Cas9 systems. His work also investigates RNA splicing as a source of biomarkers and therapeutic targets, including neo-antigens for cancer vaccines and membrane proteins for CAR-T therapy or antibody-drug conjugates.

Research topics

• Physics
• Particle physics
• Nuclear physics
• Computer Science
• Algorithm
• Quantum mechanics
• Mathematics
• Optics
• Chemistry
• Materials science
• Astrophysics
• Mathematical physics

Selected publications

• Integrative functional genomics analysis identifies pleiotropic genes for vascular diseases

  Nature Communications · 2026-02-05

  articleOpen access

  Several vascular diseases including coronary artery disease, hypertension, stroke, and abdominal aortic aneurysm, have significant genetic underpinnings. Genome-wide association studies have unveiled many genetic loci associated with one or more of these diseases. However, the causative genes at most of these loci are yet to be determined, which hampers the translation of the genetic findings into a better understanding of the disease mechanisms and the identification of new therapeutic targets. Here, in an integrative functional genomics analysis of these loci, we identify a panel of likely causal genes, some of which are pleiotropic for more than one of these vascular diseases. Pooled CRISPR knockout screen analyses of these likely causal genes indicate that many of them influence vascular smooth muscle cell behaviour, and validation experiments of selected genes confirm that FES, BCAR1, CARF and SMARCA4 exert such effects. Further functional experiments focusing on FES, a pleiotropic gene for both coronary artery disease and hypertension, show that it modulates the expression of genes involved in vascular remodeling and that Fes knockout in mice promotes atherosclerosis as well as raises blood pressure. These findings provide an insight into the genetic basis of vascular diseases and inform targets for therapeutic development.

  PublisherOA PDFDOI

• Antineutrophil Cytoplasmic Antibodies Contribute to Airway Inflammation via Induction of Neutrophil Extracellular Traps in Children With Bronchiolitis Obliterans

  The Clinical Respiratory Journal · 2026-01-01

  articleOpen access

  OBJECTIVE: It was found that the levels of antineutrophil cytoplasmic antibodies (ANCA) are elevated and linked to disease severity of bronchiolitis obliterans (BO) in children. This study aims to explore the mechanism of ANCA in the process of BO. METHODS: Plasma from BO patients (n = 40) and healthy controls (n = 11) was analyzed for ANCA and neutrophil extracellular traps (NETs) components. Plasma IgG from ANCA-positive BO children and normal controls were used to stimulate neutrophils, measuring reactive oxygen species (ROS) and NETs production. Small airway epithelial cells (SAECs) were exposed to NETs, assessing viability by CCK8 and cytokine release by ELISA. The IgG treated neutrophils were co-cultured with SAECs, and cytokines were measured by ELISA. RESULTS: The levels of ANCA and NETs components including dsDNA, neutrophil elastase (NE) and myeloperoxidase (MPO) in the plasma of BO children were significantly higher than those of healthy controls. ANCA-positive IgG induced neutrophils produce ROS and NETs. The cell viability of SAECs was significantly reduced upon treatment with NETs in a concentration-dependent manner. The levels of IL-8, IL-17, TNF-α, and TGF-β secreted by SAECs treated with NETs were increased significantly, and the degree of increase was positively correlated with the concentration of NETs. The co-culture of neutrophils stimulated by ANCA IgG with SAECs significantly increased the expression of cytokines including IL-8, IL-17, TNF-α, and TGF-β. CONCLUSIONS: NETs induced by ANCA may exacerbate airway inflammation in children with BO.

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• Abstract 2112 Transient miRISC-mRNA interactions within higher order RNP assemblies promote translational repression

  Journal of Biological Chemistry · 2025-05-01

  articleOpen access

  aptamer.The oligonucleotide pool is progressively enriched by adjusting the ratio to include more N71 RNA pool and less SOD1 target, ensuring that only the highest-affinity aptamers bind effectively.To further enhance stringency, additional washes with higher wash volumes have been implemented, increasing the selectivity for aptamer-target binding.After 5-6 rounds of SELEX, the enriched RNA pool will be cloned and sequenced after the fifth or sixth round of selection to assess whether a viable aptamer targeting SOD1 has been identified.Once a successful aptamer for SOD1 is identified, the project will move forward to develop an aptamer targeting the biomarker pirenzepine.These two aptamers will then be utilized through aptamer-based targeted delivery within a therapeutic to alleviate symptoms of multiple sclerosis.Thank you for the generous support of the UT Freshman Research Initiative in providing the laboratory resources and materials essential for conducting this project.

  PublisherOA PDFDOI

• Agarotetrol alleviates reflux esophagitis by regulating autophagy through the METTL14/FOXO3a pathway

  European Journal of Pharmacology · 2025-10-23 · 1 citations

  articleSenior authorCorresponding
  PublisherDOI

• A Mendelian randomization-based risk model using aging-related genes for prognosis in lung adenocarcinoma

  Discover Oncology · 2025-11-24

  articleOpen access

  BACKGROUND: Aging-related genes (ARGs) are prognostic markers in cancers, but their role in lung adenocarcinoma (LUAD) remains unclear. Investigating ARGs in LUAD may provide valuable insights for clinical diagnosis and treatment. METHODS: Gene expression profiles from TCGA and GEO datasets were analyzed to identify ARG-related genes. Univariate Cox regression and LASSO analysis were used to construct a prognostic risk model. Kaplan-Meier survival analysis, ROC curves, and clinicopathological features validated its predictive accuracy. Immune cell infiltration and tumor microenvironment were assessed using CIBERSORT and ESTIMATE. RT-qPCR was used to validate the differential expression of key genes in LUAD and adjacent normal tissues. RESULTS: Seven prognostic ARGs (RHPN2, BLK, PTPRO, CA4, UBE2C, METTL7A, and H2BC12) were identified. The risk model stratified patients into high- and low-risk groups, with high-risk individuals showing poorer survival, increased immune evasion, and altered immune cell infiltration. These findings were validated in independent datasets. RT-qPCR confirmed elevated RHPN2, BLK, UBE2C, and H2BC12 in tumors, while PTPRO, CA4, and METTL7A were reduced. CONCLUSION: A robust ARG-based risk model, leveraging Cox regression and LASSO, effectively predicts survival and immunotherapy responses in LUAD, offering new tools for personalized prognosis and treatment strategies.

  PublisherDOI

• A combined strategy of multi-toxin detection and ITS identification for accurate and efficient inspection of poisonous mushrooms

  Journal of Food Composition and Analysis · 2025-04-26 · 2 citations

  article
  PublisherDOI

• Cepharanthine hydrochloride inhibits prostate cancer progression by modulating gut microbiota and metabolites

  Frontiers in Pharmacology · 2025-08-13

  articleOpen access1st author

  Background Cepharanthine Hydrochloride (CH) is widely used in clinical settings to alleviate leukopenia caused by various tumors following radiotherapy and chemotherapy. However, it remains unclear whether CH have an inhibitory effect on the progression of prostate cancer, and whether this effect is mediated by gut microbiota. To address this question, the present study constructed normal mouse models of prostate cancer, as well as antibiotic-treated mouse models of prostate cancer. Methods CH were then administered via gavage to both groups of model mice. After treatment, the tumor sizes of the mice were measured, and feces, blood, and tumor tissues from both groups were collected for 16S rDNA, metabolomics, and transcriptomics sequencing analysis. Results Results showed CH treatment significantly suppressed prostate cancer growth in mice without antibiotic cocktail pretreatment, but not in antibiotic-pretreated mice. 16S rRNA sequencing revealed distinct gut microbiota alterations in CH-Ctrl versus Ctrl/CH-ABX groups, with increased g_Blautia, g_ Lactobacillus , g_Butyricicoccus and decreased g_Akkermansia abundances. Metabolomic analysis identified 240 and 123 differentially abundant metabolites in CH-Ctrl vs Ctrl and CH-ABX, respectively. RNA-seq detected 579 and 530 differentially expressed genes in CH-Ctrl vs Ctrl and CH-ABX, respectively. Correlation analysis of differential gut microbiota, metabolites, and genes suggested that CH might inhibit prostate cancer growth by increasing the relative abundance of g_Blautia, g_ Lactobacillus , and g_Butyricicoccus, suppressing g_Akkermansia proliferation, enhancing Acetylglycine metabolite production, upregulating Ttpa, Gm14964, Shc3, Elovl4 gene expression, and downregulating Gm10531, Bc021767 gene expression. Conclusion This study is the first to explore the potential mechanisms of gut microbiota-mediated CH treatment for prostate cancer, providing a scientific basis for the application of CH in PCa therapy.

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• A rationally engineered PVA-HA hydrogel orchestrates osteochondral regeneration and matrix mineralization by cytoprotecting chondrocytes mitochondrion

  Chemical Engineering Journal · 2025-08-11 · 2 citations

  article
  PublisherDOI

• The effects of two combined methods of P53 expression and preoperative serum CEA detection on the prognosis of colorectal cancer

  Frontiers in Oncology · 2025-07-21 · 1 citations

  articleOpen accessSenior author

  Aim: To explore the effects of two combined methods-P53 expression and preoperative serum carcinoembryonic antigen (S-CEA) detection-on the prognosis of colorectal cancer (CRC). Methods: Two classified combinations of tissue P53 and S-CEA were utilized: Combined P53 groups (normal P53 and S-CEA, or one or both elevated) and Recombined groups (P53 normal & S-CEA normal, P53 normal & S-CEA high, P53 high & S-CEA normal, P53 high & S-CEA high). Clinicopathologic features were analyzed by P53, S-CEA, Combined P53, and Recombined P53. Correlations between them were examined. Overall survival (OS) and disease-free survival (DFS) were evaluated using the Kaplan-Meier method and Log-Rank test. Univariate and multivariate analyses were performed for Combined P53 and Recombined P53 to determine independent factors. Three-year, two-year, and one-year OS and DFS were further analyzed using multimeROC. SPSS 27 and R 4.4.1 were used for analysis. Results: TNM stage, CA199, differentiation, tumor maximum size, and minimum size showed significant differences between the single P53 and S-CEA groups (all P < 0.05). TNM stage, CA199, and chemotherapy differed in both Combined P53 and Recombined P53 groups (all P < 0.05). Significant correlations were found between P53, S-CEA, Combined P53, and Recombined P53 (all P < 0.001). No significant differences in OS and DFS were observed with P53 and Combined P53 (all P > 0.05), but differences were noted with S-CEA and Recombined P53 (all P < 0.05). Univariate and multivariate analyses identified laparoscopy, chemotherapy, differentiation, TNM stage, and Recombined P53 as independent factors for OS and DFS, while P53, S-CEA, and Combined P53 were not. Further multimeROC analysis showed that 3-year OS had better sensitivity and specificity (Area Under Curve [AUC] = 0.54), and 1-year DFS was better (AUC = 0.59). Conclusions: Recombined P53 classification was more effective than traditional Combined P53 classification for assessing CRC prognosis and was an independent factor. Additionally, the 3-year OS and 1-year DFS analysis demonstrated higher sensitivity and specificity with Recombined P53.

  PublisherOA PDFDOI

• Single-cell perspective on the Monocyte-to-HDL cholesterol ratio as a metastasis biomarker in papillary thyroid cancer

  BMC Cancer · 2025-07-23

  articleOpen access

  BACKGROUND: Papillary thyroid carcinoma (PTC) is a globally widespread inflammation-related cancer, where lymph node metastasis (LNM) poses significant challenges to the prognosis of PTC. The role of the monocyte-to-high-density lipoprotein cholesterol ratio (MHR), a novel inflammation marker attracting increasing attention, in PTC remains unclear. METHODS: Clinical data analysis was adopted to preliminarily explore the relationship between clinical features and LNM of PTC. Single-cell RNA sequencing (scRNA-seq) data from the GSE191288 and GSE193581 datasets were integrated to analyze various single-cell infiltration in PTC. A comprehensive suite of in vitro experiments, encompassing immunohistochemistry, co-culture, and Transwell assays were conducted to elucidate the regulatory role of macrophages and PTC. RESULTS: Clinical data analysis confirmed MHR could be an independent risk factor for LNM (OR = 1.76, 95%CI: 1.20-2.88, P = 0.011). The single-cell analysis identified cell clusters associated with dysregulated cholesterol homeostasis Q1 and CD68 + C3 macrophage subpopulations, as well as their markers GDF15. Further analysis confirmed that they are closely related to PTC metastasis and malignancy, which also implied a significant correlation between MHR and LNM. The in vitro experiments demonstrated PTC may promote metastasis by mediating inducing macrophage differentiation to the M2 phenotype. CONCLUSION: This study revealed the potential role of MHR in PTC from the single-cell perspective for the first time. Combined with the results of clinical studies and basic experiments, it was confirmed that mononuclear/macrophage and cholesterol homeostasis significantly promoted the lymph node metastasis of PTC. Overall, these findings informed robust support for MHR as an emerging marker for preoperative LNM prediction of PTC.

  PublisherOA PDFDOI

Frequent coauthors

• T. Beau

  Consejo Nacional de Investigaciones Científicas y Técnicas

  6260 shared

• J. Ocariz

  Université Paris Cité

  5744 shared

• S. De Cecco

  Radboud University Nijmegen

  5729 shared

• L. Roos

  Laboratoire de Physique Nucléaire et de Hautes Énergies

  5723 shared

• S. Trincaz-Duvoid

  Laboratoire de Physique Nucléaire et de Hautes Énergies

  5691 shared

• B. Trocmé

  Laboratoire AstroParticule et Cosmologie

  5690 shared

• M. Ridel

  Université Paris Cité

  5680 shared

• P. A. Delsart

  Université Grenoble Alpes

  4790 shared

Labs

• Biochemistry and Molecular GeneticsPI

Education

• PhD

  Case Western Reserve University School of Medicine

• Postdoc

  Yale University School of Medicine