ArticleIn vitro cellular & developmental biology. Animal2020
miR-346-3p promotes osteoclastogenesis via inhibiting TRAF3 gene.
Article in In vitro cellular & developmental biology. Animal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Targeting Sphingosine-1-Phosphate Signaling Attenuates Doxorubicin-Aggravated Bone Loss in Obese Breast Cancer Mice.Smart medicine · 2026Article
- MiR-378 mediates the ovariectomy induced bone loss via exaggerating osteoclastogenesis and transforming growth factor beta impaired osteogenesis.Genes & diseases · 2026Article
- MicroRNA in prostate cancer: from biogenesis to applicative potential.BMC urology · 2024Review
- Molecular Signaling Pathways and MicroRNAs in Bone Remodeling: A Narrative Review.Diseases (Basel, Switzerland) · 2024Review
- Regulation of osteoclast-mediated bone resorption by microRNA.Cellular and molecular life sciences : CMLS · 2022Review
- MicroRNA-455-3p regulates proliferation and osteoclast differentiation of RAW264.7 cells by targeting PTEN.BMC musculoskeletal disorders · 2022Article
- Roles of MicroRNAs in Bone Destruction of Rheumatoid Arthritis.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
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.
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Registered trials
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