Autophagy-induced RelB/p52 activation mediates tumour-associated macrophage repolarisation and suppression of hepatocellular carcinoma by natural compound baicalin

Keyphrases

• Hepatocellular Carcinoma 100%
• Autophagy 100%
• Baicalin 100%
• Natural Compounds 100%
• RelB 100%
• Tumor-associated Macrophage Repolarization 100%
• Macrophage Suppression 100%
• Tumor-associated Macrophages 66%
• Macrophages 25%
• M1-like 25%
• Repolarization 25%
• Hepatocellular Carcinoma Cells 16%
• Clodronate 16%
• Oral Administration 8%
• Liposomes 8%
• Macrophage Polarization 8%
• Macrophage-like 8%
• Suppression Effect 8%
• Transcriptional Activation 8%
• Autophagy Pathway 8%
• Microenvironment 8%
• Motility 8%
• M2 Macrophages 8%
• M1 Phenotype 8%
• Minimal Impact 8%
• Tumor-associated 8%
• TRAF2 8%
• Conditioned Medium 8%
• Macrophage Populations 8%
• Specific Toxicity 8%
• Mouse Macrophages 8%
• Orthotopic Hepatocellular Carcinoma 8%
• Inflammatory Cytokine Response 8%
• M2-like 8%
• Tumor Regression 8%
• Autophagic Degradation 8%
• Bone Marrow-derived Monocytes 8%
• Immune-competent 8%
• Polarization Factor 8%
• Macrophage Reprogramming 8%

Pharmacology, Toxicology and Pharmaceutical Science

• Natural Product 100%
• Neoplasm 100%
• Baicalin 100%
• Liver Cell Carcinoma 100%
• Clodronic Acid 16%
• Cytokine 8%
• Liposome 8%
• Tumor Regression 8%
• Tumor Necrosis Factor Receptor Associated Factor 2 8%

Immunology and Microbiology

• Autophagy 100%
• Tumor-Associated Macrophage 100%
• Repolarization 100%
• Macrophage 58%
• Carcinoma Cell 16%
• Coculture 8%
• Immunity 8%
• Proinflammatory Cytokine 8%
• Cytokine Production 8%
• Transactivation 8%
• Transcription Initiation 8%