A5071806315- Cancer Research and Treatments
- Metabolism and Genetic Disorders
- Cancer, Hypoxia, and Metabolism
- Peptidase Inhibition and Analysis
- Epigenetics and DNA Methylation
- Cancer-related gene regulation
- Ubiquitin and proteasome pathways
- Liver Disease Diagnosis and Treatment
- Protein Degradation and Inhibitors
- Amino Acid Enzymes and Metabolism
- Biochemical and Molecular Research
- Nitric Oxide and Endothelin Effects
- Histone Deacetylase Inhibitors Research
- Covalent Organic Framework Applications
- Inflammatory Bowel Disease
- Traditional Chinese Medicine Analysis
- Endoplasmic Reticulum Stress and Disease
- Protein Kinase Regulation and GTPase Signaling
- Advanced Photocatalysis Techniques
- Hepatocellular Carcinoma Treatment and Prognosis
- Gut microbiota and health
- PI3K/AKT/mTOR signaling in cancer
- Glioma Diagnosis and Treatment
- Inflammasome and immune disorders
- Genomics, phytochemicals, and oxidative stress
University of California, San Diego
2024-2025
Chinese Academy of Sciences
2019-2024
University of Chinese Academy of Sciences
2019-2024
Shanghai Institute of Materia Medica
2019-2024
Moores Cancer Center
2024
The metabolic landscape of cancer greatly influences antitumor immunity, yet it remains unclear how organ-specific metabolites in the tumor microenvironment influence immunosurveillance. We found that accumulation primary conjugated and secondary bile acids (BAs) are features human hepatocellular carcinoma experimental liver models. Inhibiting BA synthesis hepatocytes through deletion BA-conjugating enzyme acid–CoA:amino acid N -acyltransferase (BAAT) enhanced tumor-specific T cell...
Abstract One of the biggest hurdles for development metabolism-targeted therapies is to identify responsive tumor subsets. However, metabolic vulnerabilities most human cancers remain unclear. Establishing link between signatures and oncogenic alterations receptor tyrosine kinases (RTK), well-defined cancer genotypes, may precisely direct intervention a broad patient population. By integrating metabolomics transcriptomics, we herein show that RTK activation causes distinct preference....
The urea cycle is frequently rewired in cancer cells to meet the metabolic demands of cancer. Elucidation underlying mechanism by which oncogenic signaling mediates reprogramming could help identify targetable vulnerabilities. In this study, we discovered that activation KRAS non-small cell lung (NSCLC) silenced expression argininosuccinate synthase 1 (ASS1), a enzyme catalyzes production arginine from aspartate and citrulline, thereby diverted utilization pyrimidine synthesis high demand...
It remains a big challenge to develop HDAC inhibitors effective for solid tumors. Previous studies have suggested that the feedback activation of JAK-STAT3 pathway represents key mechanism leading resistance in breast cancer, suggesting therapeutic promise JAK/HDAC dual inhibitors. In this work, we discovered series pyrrolo[2,3-d]pyrimidine-based derivatives as potent JAK and Especially, compounds 15d 15h potently inhibited JAK1/2/3 HDAC1/6 displayed antiproliferative proapoptotic activities...
Abstract Intervention of the gut microbiome is a promising adjuvant strategy in cancer immunotherapy. Chemotherapeutic agents are recognized for their substantial impacts on microbiome, yet therapeutic potential as modulators remains uncertain, due to complexity microbiome‐host‐drug interactions. Here, it showed that low‐dose chemotherapy preferentially shapes ileal augment extraintestinal immune response anti‐programmed death‐1 (anti‐PD‐1) therapy without causing intestinal toxicity....
The chemical carcinogen diethylnitrosamine (DEN) is often used to induce HCC in mice. Curiously, several labs have reported that the removal of oncoproteins from hepatocytes exacerbated DEN-induced HCC, with mechanisms unknown. This study aimed at deciphering molecular underlying tumor suppressive effect oncoproteins.
Abstract Hepatocellular carcinoma (HCC) is one of the most common causes cancer-related death without effective treatment. Oncogenic drivers, including PTPN11/Shp2, Ikkβ kinase (IKK), c-Met and β-catenin, as well tumor microenvironment illustrated by a carcinogen or diethylnitrosamine (DEN)-treated models, have combined contribution to cancer progression that distinct prevalence in human HCC progression. We previously found disruption Ras/Erk Shp2 deletion with NF-κB unexpectedly...
<p>Differential gene expression of BEAS-2B cells expressing KRAS-G12D or empty vector control</p>
<p>Supplementary figure S1-5</p>
<div>Abstract<p>The urea cycle is frequently rewired in cancer cells to meet the metabolic demands of cancer. Elucidation underlying mechanism by which oncogenic signaling mediates reprogramming could help identify targetable vulnerabilities. In this study, we discovered that activation KRAS non–small cell lung (NSCLC) silenced expression argininosuccinate synthase 1 (ASS1), a enzyme catalyzes production arginine from aspartate and citrulline, thereby diverted utilization...
<div>Abstract<p>The urea cycle is frequently rewired in cancer cells to meet the metabolic demands of cancer. Elucidation underlying mechanism by which oncogenic signaling mediates reprogramming could help identify targetable vulnerabilities. In this study, we discovered that activation KRAS non–small cell lung (NSCLC) silenced expression argininosuccinate synthase 1 (ASS1), a enzyme catalyzes production arginine from aspartate and citrulline, thereby diverted utilization...
<p>Differential gene expression of BEAS-2B cells expressing KRAS-G12D or empty vector control</p>
<p>Supplementary figure S1-5</p>
Pharmacological perturbation studies based on protein-level signatures are fundamental for drug discovery. In the present study, we used a mass spectrometry (MS)-based proteomic platform to profile whole proteome of breast cancer MCF7 cell line under stress induced by 78 bioactive compounds. The integrated analysis perturbed signal abundance revealed connectivity between phenotypic behaviors and molecular features in cells. Our data showed functional relevance exploring novel pharmacological...