Myct1 as a contact point of TGF-beta and c-Myc; analysis of the function

2016 Fiscal Year Final Research Report

• Project/Area Number: 26462307
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: Kagoshima University
• Principal Investigator: Ishidou Yasuhiro 鹿児島大学, 医歯学総合研究科, 特任准教授 (10300740)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: TGF-β / 軟骨細胞分化 / Myct1

Outline of Final Research Achievements

During endochondral ossification process, TGF-β signaling promotes chondrocyte differentiation while inhibits hypertrophic chondrocyte maturation, which underlying mechanisms are not clear. We found that TGF-β1 strongly induced expression of Myct1 gene in human chondrocyte cell line. siRNA-mediated knockdown of c-Myc diminished TGF-β1-induced Myct1 expression, suggesting that c-Myc is indispensable for the expression. However, silencing of Myct1 did not affect TGF-β1-mediated chondrocyte differentiation. Then, we next focused on PEG10 gene which was suppressed by TGF-β1. Induction of PEG10 inhibited TGF-β signaling, suggesting PEG10 to be a novel inhibitory factor for TGF-β pathway.

Free Research Field

股関節外科