miR‑382 inhibits breast cancer progression and metastasis by affecting the M2 polarization of tumor‑associated macrophages by targeting PGC‑1α

Macrophage polarization Ectopic expression M2 Macrophage
DOI: 10.3892/ijo.2022.5416 Publication Date: 2022-09-06T09:43:48Z
ABSTRACT
Macrophages are principal immune cells with a high plasticity in the human body that can differentiate under different conditions tumor microenvironment to adopt two polarized phenotypes opposite functions. Therefore, converting macrophages from immunosuppressive phenotype (M2) inflammatory (M1) is considered promising therapeutic strategy for cancer. However, molecular mechanisms underlying this conversion process have not yet been completely elucidated. In recent years, microRNAs (miRNAs or miRs) shown play key roles regulating macrophage polarization through their ability modulate gene expression. present study, it was found miR‑382 expression significantly downregulated tumor‑associated (TAMs) and M2‑polarized breast <em>In vitro</em>, toward M2 M2‑type cytokine release were inhibited by transfection miR‑382‑overexpressing lentivirus. Similarly, overexpression of TAMs promote malignant behaviors cancer cells. addition, peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) identified as downstream target PGC‑1α affected altering metabolic status. The ectopic restored secretion macrophages. Furthermore, reversed miR‑382‑induced changes state effects on Of note, <em>in vivo</em> growth metastasis 4T1 TAMs. Taken together, results study suggest may alter status targeting PGC‑1α, thereby decreasing proportion phenotype, inhibiting progression
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