A5085648672- Cancer, Hypoxia, and Metabolism
- Lung Cancer Treatments and Mutations
- Growth Hormone and Insulin-like Growth Factors
- Cytokine Signaling Pathways and Interactions
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Cancer Mechanisms and Therapy
- Synthesis and biological activity
- Ocular Oncology and Treatments
- Cardiac Fibrosis and Remodeling
- Immune Cell Function and Interaction
- PI3K/AKT/mTOR signaling in cancer
- Calcium signaling and nucleotide metabolism
- Advanced biosensing and bioanalysis techniques
- Gold and Silver Nanoparticles Synthesis and Applications
- Dendrimers and Hyperbranched Polymers
- Phagocytosis and Immune Regulation
- Sirtuins and Resveratrol in Medicine
- Atherosclerosis and Cardiovascular Diseases
- Multiple Myeloma Research and Treatments
- Biomarkers in Disease Mechanisms
- Developmental Biology and Gene Regulation
- Retinal Development and Disorders
- HER2/EGFR in Cancer Research
- Peptidase Inhibition and Analysis
Sun Yat-sen University
2020-2025
Dongguan People’s Hospital
2023
Southern Medical University
2022
Shandong University
2021
Chemotherapy is still one of the principal treatments for gastric cancer, but clinical application 5-FU limited by drug resistance. Here, we demonstrate that ferroptosis triggered STAT3 inhibition may provide a novel opportunity to explore new effective therapeutic strategy cancer and chemotherapy We find negative regulation (FNR) signatures are closely correlated with progression chemoresistance cancer. FNR associated genes (GPX4, SLC7A11, FTH1) upregulated in resistant cells xenografts....
Abstract Acquired resistance represents a bottleneck for effective molecular targeted therapy in lung cancer. Metabolic adaptation is distinct hallmark of human cancer that might contribute to acquired resistance. In this study, we discovered novel mechanism EGFR tyrosine kinase inhibitors (TKI) mediated by IGF2BP3-dependent cross-talk between epigenetic modifications and metabolic reprogramming through the IGF2BP3–COX6B2 axis. IGF2BP3 was upregulated patients with TKI-resistant non–small...
Constitutive activation of signal transducer and activator transcription 3 (STAT3) is a common feature in human non-small cell lung cancer (NSCLC).STAT3 plays an important role progression as driver oncogene acquired resistance targeted therapies alternatively activated pathway.W2014-S with pharmacophore structure imidazopyridine, which was firstly reported to be utilized STAT3 inhibitor discovery, screened out potent from library small molecules.The aim this study investigate the antitumor...
Abstract Background Metastasis is the primary cause of mortality in small cell lung cancer (SCLC), with liver being a predominant site for distal metastasis. Despite this clinical significance, mechanisms underlying interaction between SCLC and microenvironment, fostering metastasis, remain unclear. Methods patient tissue array, bioinformatics analysis were performed to demonstrate role periostin (POSTN) progression, prognosis. Cell migration, invasion sphere formation assay determine...
Constitutively activated G proteins caused by specific mutations mediate the development of multiple malignancies. The mutated Gαq/11 are perceived as oncogenic drivers in vast majority uveal melanoma (UM) cases, making directly targeting to be a promising strategy for combating UM. Herein, we report optimization imidazopiperazine derivatives inhibitors, and identified GQ262 with improved inhibitory activity drug-like properties. efficiently blocked UM cell proliferation migration vitro....
Abstract Uveal melanoma (UM), the predominant primary ocular malignancy, often progresses to liver metastasis with limited therapeutic options. The interplay of tumor microenvironment, encompassing secreted soluble factors, plays a crucial role in facilitating metastasis. In this study, is elucidated neural growth factor‐inducible gene (VGF), neuropeptide precursor, Gαq mutant UM. Employing multiomics approach, transcriptomic and secretomic analyses, intricate involvement VGF UM progression...
Objective. To investigate the mechanism of Connexin 37 (Cx37) and Kv1.3 pathways in atherosclerosis (AS). Methods. ApoE-/- mice were given a high-fat diet to establish (AS) model, macrophages isolated extracted transfect Cx37 vectors with silencing or overexpressing, pathway blockers used inhibit activity. The indexes body weight, blood glucose, lipid collected. protein mRNA expression levels detected by reverse transcription-PCR (RT-PCR), Western blot, immunofluorescence technique. Oil red...
SH2 domains have been recognized as promising targets for various human diseases. However, targeting with phosphopeptides or small-molecule inhibitors derived from bioisosteres of the phosphate group is still challenging. Identifying novel to achieve favorable in vivo potency urgently needed. Here, we report feasibility STAT3-SH2 domain a boronic acid and identification highly potent inhibitor compound 7 by replacing carboxylic 4 acid. Compound shows higher binding affinity, better cellular...
Nanomedicine has made great progress in the targeted therapy of cancer. Here, we established a novel drug-mate strategy by studying formulation nanodrugs at molecular level. In combination, drug is hydrophobic that poorly soluble water, and mate an amphiphilic small molecule (SMA) both hydrophilic lipophilic properties. We proposed could co-assemble with suitable SMA on nanoscale without additive agents. The proof-of-concept methodology results were presented to support our hypothesis....
<p>Supplementary Data</p>
<p>Supplementary Data</p>
<div>Abstract<p>Acquired resistance represents a bottleneck for effective molecular targeted therapy in lung cancer. Metabolic adaptation is distinct hallmark of human cancer that might contribute to acquired resistance. In this study, we discovered novel mechanism EGFR tyrosine kinase inhibitors (TKIs) mediated by IGF2BP3-dependent crosstalk between epigenetic modifications and metabolic reprogramming through the IGF2BP3-COX6B2 axis. IGF2BP3 was upregulated TKI-resistant...
Abstract Acquired resistance represents a bottleneck to molecular targeted therapy in lung cancer. Metabolic adaptation is distinct hallmark of human cancer, but its role acquired has not been fully understood. In this study, we discovered novel mechanism TKI involved IGF2BP3-dependent crosstalk between the epigenetic modifications and metabolic reprogramming through IGF2BP3-COX6B2 axis. We demonstrated upregulated expression RNA binding protein IGF2BP3 reduced sensitivity treatment...
<p>Supplementary Data</p>
<p>Supplementary Data</p>
<div>Abstract<p>Acquired resistance represents a bottleneck for effective molecular targeted therapy in lung cancer. Metabolic adaptation is distinct hallmark of human cancer that might contribute to acquired resistance. In this study, we discovered novel mechanism EGFR tyrosine kinase inhibitors (TKI) mediated by IGF2BP3-dependent cross-talk between epigenetic modifications and metabolic reprogramming through the IGF2BP3–COX6B2 axis. IGF2BP3 was upregulated patients with...
<div>Abstract<p>Acquired resistance represents a bottleneck for effective molecular targeted therapy in lung cancer. Metabolic adaptation is distinct hallmark of human cancer that might contribute to acquired resistance. In this study, we discovered novel mechanism EGFR tyrosine kinase inhibitors (TKIs) mediated by IGF2BP3-dependent crosstalk between epigenetic modifications and metabolic reprogramming through the IGF2BP3-COX6B2 axis. IGF2BP3 was upregulated TKI-resistant...