論文

国際誌
2013年1月11日

TFE3 inhibits myoblast differentiation in C2C12 cells via down-regulating gene expression of myogenin.

Biochemical and biophysical research communications
  • Ayano Naka
  • ,
  • Kaoruko Tada Iida
  • ,
  • Yoshimi Nakagawa
  • ,
  • Hitoshi Iwasaki
  • ,
  • Yoshinori Takeuchi
  • ,
  • Aoi Satoh
  • ,
  • Takashi Matsuzaka
  • ,
  • Kiyo-Aki Ishii
  • ,
  • Kazuto Kobayashi
  • ,
  • Shigeru Yatoh
  • ,
  • Masako Shimada
  • ,
  • Naoya Yahagi
  • ,
  • Hiroaki Suzuki
  • ,
  • Hirohito Sone
  • ,
  • Nobuhiro Yamada
  • ,
  • Hitoshi Shimano

430
2
開始ページ
664
終了ページ
9
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2012.11.094

Transcription factor E3 (TFE3) belongs to a basic helix-loop-helix family, and is involved in the biology of osteoclasts, melanocytes and their malignancies. We previously reported the metabolic effects of TFE3 on insulin in the liver and skeletal muscles in animal models. In the present study, we explored a novel role for TFE3 in a skeletal muscle cell line. When TFE3 was overexpressed in C2C12 myoblasts by adenovirus before induction of differentiation, myogenic differentiation of C2C12 cells was significantly inhibited. Adenovirus-mediated TFE3 overexpression also suppressed the gene expression of muscle regulatory factors (MRFs), such as MyoD and myogenin, during C2C12 differentiation. In contrast, knockdown of TFE3 using adenovirus encoding short-hairpin RNAi specific for TFE3 dramatically promoted myoblast differentiation associated with significantly increased expression of MRFs. Consistent with these findings, promoter analyses via luciferase reporter assay and electrophoretic mobility shift assay suggested that TFE3 negatively regulated myogenin promoter activity by direct binding to an E-box, E2, in the myogenin promoter. These findings indicated that TFE3 has a regulatory role in myoblast differentiation, and that transcriptional suppression of myogenin expression may be part of the mechanism of action.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2012.11.094
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/23211595
ID情報
  • DOI : 10.1016/j.bbrc.2012.11.094
  • PubMed ID : 23211595

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