MicroRNAs (miRNAs) modulate gene expression and regulate many physiological and pathological conditions. However, their modulation and effect in osteoclastogenesis remain unknown. In this study, we investigated the role of miR-346-3p in regulating the osteoclast differentiation from RAW264.7 cells. We used the miRNA microarray assay, miR-346-3p mimic transfection, tartrate resistant acid phosphatase (TRAP) staining, bone resorption assay, qRT-PCR, and western blot. Our results showed that the expression of miR-346-3p was significantly upregulated during osteoclast differentiation. Further, by transfecting cells with miR-346-3p mimic, we observed an increased number of TRAP-positive multinucleated cells, increased pit area caused by bone resorption, and enhanced expression of osteoclast-specific genes and proteins. Conversely, miR-346-3p inhibition attenuated the osteoclast differentiation and function. Software-mediated prediction and validation using luciferase reporter assay showed that TRAF3, a negative regulator of osteoclast differentiation, was inhibited by miR-346-3p overexpression. Our results showed that miR-346-3p directly targeted TRAF3 mRNA via binding to its 3′-UTR and inhibited the expression of TRAF3 protein. Taken together, our results revealed that miR-346-3p promotes the regulation of osteoclastogenesis by suppressing the TRAF3 gene. In conclusion, miR-346-3p could be a novel therapeutic target for bone loss-related pathogenesis.

MicroRNA（miRNA）调节基因表达并调节许多生理和病理状况。然而，它们在破骨细胞形成中的调节和作用仍然未知。在这项研究中，我们研究了miR-346-3p在调节破骨细胞从RAW264.7细胞分化中的作用。我们使用了miRNA芯片检测，miR-346-3p模拟转染，酒石酸抗性酸性磷酸酶（TRAP）染色，骨吸收检测，qRT-PCR和Western blot。我们的结果表明，在破骨细胞分化过程中，miR-346-3p的表达明显上调。此外，通过用miR-346-3p模拟物转染细胞，我们观察到TRAP阳性多核细胞数量增加，骨吸收引起的凹坑面积增加，破骨细胞特异性基因和蛋白质的表达增强。反过来，miR-346-3p抑制减弱了破骨细胞的分化和功能。软件介导的预测和使用萤光素酶报告基因检测的验证表明，miR-346-3p过表达抑制破骨细胞分化的负调节剂TRAF3。我们的结果表明，miR-346-3p通过与其3'-UTR结合直接靶向TRAF3 mRNA，并抑制TRAF3蛋白的表达。两者合计，我们的结果表明，miR-346-3p通过抑制TRAF3基因来促进破骨细胞的调节。总之，miR-346-3p可能是骨丢失相关发病机制的新型治疗靶标。被miR-346-3p过表达抑制。我们的结果表明，miR-346-3p通过与其3'-UTR结合直接靶向TRAF3 mRNA，并抑制TRAF3蛋白的表达。两者合计，我们的结果表明，miR-346-3p通过抑制TRAF3基因来促进破骨细胞的调节。总之，miR-346-3p可能是骨丢失相关发病机制的新型治疗靶标。被miR-346-3p过表达抑制。我们的结果表明，miR-346-3p通过与其3'-UTR结合直接靶向TRAF3 mRNA，并抑制TRAF3蛋白的表达。两者合计，我们的结果表明，miR-346-3p通过抑制TRAF3基因来促进破骨细胞的调节。总之，miR-346-3p可能是骨丢失相关发病机制的新型治疗靶标。