ArticleInternational journal of molecular sciences2026
Microbial-Derived Daidzin (Eco-3) Suppresses RANKL-Induced Osteoclastogenesis by Targeting the TBK1-NFATc1 Signaling Axis.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Eco-3, a microbial-derived daidzin, has been reported to possess diverse biological activities; however, its effects on osteoclast differentiation and the underlying molecular mechanisms remain unclear. In the present study, we investigated the effects of Eco-3 on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and explored the signaling pathways involved using RAW264.7 macrophages. Eco-3 suppressed RANKL-induced osteoclast formation at the concentrations tested without significantly affecting cell viability. Eco-3 also altered F-actin organization and reduced the expression of key osteoclastogenic markers, including tartrate-resistant acid phosphatase (TRAP), nuclear factor of activated T cells c1 (NFATc1), c-Fos, and cathepsin K (CTSK). In particular, Eco-3 attenuated NFATc1 expression during the early stage of osteoclast differentiation, suggesting interference with the transcriptional program associated with osteoclastogenesis. Furthermore, RANKL stimulation progressively increased TANK-binding kinase 1 (TBK1) phosphorylation during osteoclast differentiation, whereas Eco-3 attenuated this activation. Genetic silencing of TBK1 suppressed osteoclast formation, while pharmacological inhibition of TBK1 reduced TBK1 phosphorylation, osteoclastogenic gene expression, and osteoclast formation. Collectively, these findings suggest that Eco-3 suppresses RANKL-induced osteoclastogenesis, at least in part, through modulation of the TBK1-NFATc1 signaling axis in RAW264.7 macrophages. Our findings identify TBK1 as a potential regulatory component of osteoclast differentiation and suggest that Eco-3 warrants further investigation as a potential bioactive candidate for osteoclast-related bone disorders.
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