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Fig. 6
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.
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