ArticleBioengineered2022
Interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) accelerates osteoclast formation by regulating signal transducer and activator of transcription 3 (STAT3) signalling.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Myeloma-derived exosomal circ_0002724 promotes osteoclastogenesis through a miR-4753-3p/IFIT1 and RANK axis in myeloma bone disease.Frontiers in oncology · 2026Article
- Single-cell landscape of immunological responses in patients with juvenile idiopathic arthritis.Genes & diseases · 2025Article
- Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor.Nature biomedical engineering · 2024Article
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Abstract
Osteoclasts (OCs), the main cause of bone resorption irregularities, may ultimately cause various bone diseases, including osteoarthritis. The objective of this study was to investigate the effect of interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) on OC formation induced by receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) and to further explore its underlying mechanism. IFIT1 expression in Raw264.7 cells treated with macrophage colony-stimulating factor (M-CSF) and RANKL was determined by qRT-PCR. OC formation was detected using tartrate-resistant acid phosphatase (TRAP) staining. The effect of IFIT1 on STAT3 activation was detected using Western blotting. Additionally, Western blotting was used to measure the change in the expression of OC-specific proteins. IFIT1 was highly expressed in Raw264.7 cells after stimulation with M-CSF and RANKL. IFIT1 overexpression accelerated the formation of OCs, as evidenced by the increased number and size of multinuclear cells, and the upregulation of OC-specific proteins, and activated the STAT3 pathway, by inducing phosphorylation of JAK1 and STAT3. However, silencing of IFIT1 inhibited the formation of OCs and a STAT3 inhibitor Stattic weakened the effects of IFIT1. In conclusion, IFIT1 accelerates the formation of OCs, which is caused by RANKL by STAT3 pathway regulation. This study provides a potential basis for further research and for development of drugs for treating bone resorption-related diseases.
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