Fig. 5

Anti‐miR‐210‐3p LNA delivery increases macrophage burden promoting tumor regression in the A549 lung cancer xenograft zebrafish model. (A) Schematic diagram representing experimental design indicating days of zebrafish A549 tumor xenograft model development followed by the administration of anti‐miR‐210‐3p LNA and collection of tumor tissue and blood samples from zebrafish. (B) Representative images of A549 tumor xenograft zebrafish (day 14/control) treated without or with anti‐miR‐210‐3p LNA for indicated timepoints (left panel) (n = 4) and the representative images of harvested tumors from these zebrafish (right panel). (C,D) Relative tumor growth (%) (C) and tumor weight (mg) (D) after treatment with anti‐miR‐210 LNA at indicated timepoints. (E,F) RT‐qPCR analysis of mir‐210‐3p (E) and CCL2 (F) gene expression in tumor xenografts treated without or with anti‐miR‐210‐3p LNA and harvested at day 3 (+d3) and day 5 (+d5) post‐treatment. U6 snRNA and β‐actin were used as loading controls for mir‐210‐3p and CCL2 gene expression normalization. (G,H) RT‐qPCR analysis showing relative abundance of MPEG1.1 (G) and MPX (H) mRNA levels in tumor xenografts treated without or with anti‐miR‐210‐3p LNA for day 3 (+d3) and day 5 (+d5). β‐actin was used as a loading control for gene expression normalization. Data represented as mean ± SD. Statistical significance was analyzed by Student's t‐test, *P < 0.05, **P < 0.01, ***P < 0.001 vs control; ^#P < 0.05, ^##P < 0.01 vs +d3; ns, nonsignificant.