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Snhg18 regulates Yap subcellular localization to maintain bone homeostasis
Jie Huang1,2, Yuteng Weng1,2, Yanhuizhi Feng1,2
1Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology, Shanghai, China.
Nature Communications
|August 14, 2025
Summary
Small nucleolar RNA host gene 18 (lnc-Snhg18) promotes bone formation by enabling Yap nuclear translocation in bone marrow stromal cells. Restoring lnc-Snhg18 levels can reverse bone loss in osteoporosis models.
Area of Science:
- Bone biology
- Cell signaling
- RNA biology
Background:
- Osteoporosis treatments often fail to restore lost bone mass.
- Yes-associated protein (Yap) nuclear translocation is vital for bone formation but impaired in osteoporosis.
- The role of long non-coding RNAs (lncRNAs) in regulating Yap signaling in osteoporosis is not fully understood.
Purpose of the Study:
- To identify novel regulators of Yap signaling in bone marrow stromal cells (BMSCs) under osteoporotic conditions.
- To investigate the role of lnc-Snhg18 in osteogenesis and its potential as a therapeutic target for osteoporosis.
Main Methods:
- Identification and characterization of lnc-Snhg18 in bone marrow stromal cells.
- Investigation of the molecular mechanism of lnc-Snhg18 in regulating Yap localization.
- Assessment of lnc-Snhg18's effect on bone mass and Yap signaling in osteoporosis models.
Main Results:
- lnc-Snhg18 is identified as a key regulator promoting osteogenesis by facilitating Yap nuclear translocation.
- lnc-Snhg18 directly binds Caveolin-1 and 14-3-3 eta protein, disrupting the 14-3-3 eta-Yap interaction.
- Knockout of lnc-Snhg18 exacerbates bone loss, while its delivery restores bone mass in osteoporosis models.
Conclusions:
- lnc-Snhg18 is a critical mediator of osteogenic differentiation and Yap signaling in bone.
- lnc-Snhg18 represents a promising therapeutic target for treating osteoporosis and related bone disorders.
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