FIGURE
            Fig. 6
- ID
 - ZDB-FIG-240509-51
 - Publication
 - Arora et al., 2022 - Hypoxia-induced miR-210-3p expression in lung adenocarcinoma potentiates tumor development by regulating CCL2-mediated monocyte infiltration
 - Other Figures
 - All Figure Page
 - Back to All Figure Page
 
                
                    
                        Fig. 6
                    
                    
                
                
            
        
        
    
        
            
            
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 Model representing miR‐210‐3p as a potential therapeutic target for lung adenocarcinoma. Left panel: LUAD solid tumor exhibits hypoxia‐associated stabilization of HIF‐1A, which by promoting miR‐210‐3p level directly involved in downregulation of CCL2 and macrophage infiltration and also favors macrophage TAM phenotype supporting tumor progression. Right panel: Therapeutic intervention of anti‐miR210‐3p LNA augment CCL2 mediated monocyte infiltration and skewing towards macrophage antitumoral M1 phenotype leading to tumor regression.  | 
    
                
                    
                        Expression Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Expression Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Antibody Labeling
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Phenotype Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Phenotype Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Acknowledgments
                    
                    
                
                
            
        
        
    
        
            
            
                
                    
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      Full text @ Mol. Oncol.