ArticleMedical oncology (Northwood, London, England)2013
Smad3 is the key to transforming growth factor-β1-induced osteoclast differentiation in giant cell tumor of bone.
Article in Medical oncology (Northwood, London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 14 citations in OpenAlex.
- p-Smad3 differentially regulates the cytological behavior of osteoclasts before and after osteoblasts maturation.Molecular biology reports · 2024Article
- SIS3, a specific inhibitor of Smad3 reverses ABCB1- and ABCG2-mediated multidrug resistance in cancer cell lines.Cancer letters · 2018Article
- TGF-βRI kinase activity mediates Emdogain-stimulated in vitro osteoclastogenesis.Clinical oral investigations · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Giant cell tumor (GCT) of bone is a benign but locally aggressive neoplasm of bone. However, molecular mechanisms underlying osteolysis in GCT have not been deeply understood. The aim of this study was to investigate one of the possible mechanisms underlying the up-regulation of receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG) expression. First, we performed an immunohistochemical study on transforming growth factor-β1 (TGF-β1) expression in 83 cases with GCT and found that increased TGF-β1 staining was significantly correlated with Campanacci stages(Spearman's correlation = 0.335, p = 0.002). Next, we investigated the mechanism of the effect of TGF-β1 on osteolysis of GCT and examined the effects of TGF-β1 plus or minus specific inhibitor of Smad3 (SIS3) on the expression of RANKL/OPG ratio at the mRNA and protein levels in two primary GCT cell lines. The results clearly indicated that TGF-β1 is capable of significantly increasing RANKL/OPG ratio (p GCT1 = 0.000, p GCT2 = 0.000) and that SIS3 is capable of reversing the ratio, suggesting that Smad3 is the key to TGF-β1-induced increased the ratio. In the co-culture system, we found that SIS3 reversed the effects of TGF-β1-induced osteoclast formation in the co-culture system (p GCT1 = 0.000, p GCT2 = 0.000). Our findings indicate that TGF-β1 plays an important role in the osteolysis of GCT via Smad3.
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