Breast cancer is becoming a common life‐threatening disease, especially in women, along with higher incidence and mortality. MicroRNA (miR)−506 was reported to participate in breast cancer progression, while the role… Click to show full abstract
Breast cancer is becoming a common life‐threatening disease, especially in women, along with higher incidence and mortality. MicroRNA (miR)−506 was reported to participate in breast cancer progression, while the role of miR‐506 in breast cancer‐induced osteolytic bone metastasis is unclear. In the present study, we found significant downregulation of miR‐506 in breast cancer tissues and cell lines. Overexpression of miR‐506 notably reduced the proliferative, migratory and invasive rates of MCF7 and MDA‐MB‐231 cells, and reduced the production of inflammatory factors IL‐6 and TNF‐α in MCF7 cells. Moreover, overexpression of miR‐506 obviously inhibited tumor growth in an in vivo animal model. In addition, overexpression of miR‐560 efficiently attenuated breast cancer‐induced osteolysis in vivo, which was characterized by increased bone volume/total volume (BT/TV), trabecular number (Tb. N), and trabecular thickness (Tb. Th), as well as the reduced trabecular separation (Tb. Sp). The nuclear factor of activated T cell cytoplasmic 1 (NFATc1) was identified as a downstream target of miR‐506, and overexpression of miR‐506 could inhibit breast cancer progression by targeting NFATc1. Furthermore, our results showed that NFATc‐1 might participate in the inhibition of miR‐506 on breast cancer‐induced osteolysis. In conclusion, our findings provide insights into understanding the pathogenesis of breast cancer and breast cancer‐induced osteolytic bone metastasis, and miR‐506 might serve as a novel biomarker for this disease.
               
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