TGF-B in jaw tumor fluids induces RANKL expression in stromal fibroblasts.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25893125
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Surgical dentistry
• Research Institution: Okayama University (2014-2015); Osaka University (2013)
• Principal Investigator: Yamada Chiaki 岡山大学, 医歯(薬)学総合研究科, 助教 (80548818)
• Project Period (FY): 2013-08-30 – 2016-03-31
• Keywords: 歯原性腫瘍 / 角化嚢胞性歯原性腫瘍 / エナメル上皮腫 / TGF-β / IL-１α / RANKL

Outline of Final Research Achievements

Odontogenic tumor, especially Ameloblastomas and KCOT develop in the jaw bone along with bone resorption. The mechanism involves the wide reception of compression-induced bone resorption associated with tumor growth. However,the mechanism of bone resorption in early-stage lesions may not be caused by compression-induced bone resorption.We hypothesized that bone resorption occurs because of RANKL expression mediation in stromal fibroblasts in the jaw bone. In the present study,the expression of TGF-β and IL-1α in odontogenic tumor cells, high concentration of TGF-β in lesion fluid, and synergistic induction of RANKL expression in stromal fibroblasts by TGF-β and IL-1α have been observed. Our results revealed the following two mechanisms: in stromal fibroblasts, TGF-β (1) promotes IL-1 signal-induced NF-κB phosphorylation and promotes RANKL expression and (2) promotes human RANKL transcription activity.

Free Research Field

顎骨良性腫瘍