PPARγ ligands suppress the feedback loop between E2F2 and cyclin-E1

Yoko Komatsu, Ichiaki Ito, Mitsutoshi Wayama, Akiko Fujimura, Kensuke Akaogi, Hikaru Machida, Yuka Nakajima, Takao Kuroda, Kazuji Ohmori, Akiko Murayama, Keiji Kimura, Junn Yanagisawa

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

PPARγ is a nuclear hormone receptor that plays a key role in the induction of peroxisome proliferation. A number of studies showed that PPARγ ligands suppress cell cycle progression; however, the mechanism remains to be determined. Here, we showed that PPARγ ligand troglitazone inhibited G1/S transition in colon cancer cells, LS174T. Troglitazone did not affect on either expression of CDK inhibitor (p18) or Wnt signaling pathway, indicating that these pathways were not involved in the troglitazone-dependent cell cycle arrest. GeneChip and RT-PCR analyses revealed that troglitazone decreased mRNA levels of cell cycle regulatory factors E2F2 and cyclin-E1 whose expression is activated by E2F2. Down-regulation of E2F2 by troglitazone results in decrease of cyclin-E1 transcription, which could inhibit phosphorylation of Rb protein, and consequently evoke the suppression of E2F2 transcriptional activity. Thus, we propose that troglitazone suppresses the feedback loop containing E2F2, cyclin-E1, and Rb protein.

Original languageEnglish (US)
Pages (from-to)145-148
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume370
Issue number1
DOIs
StatePublished - May 23 2008
Externally publishedYes

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Keywords

  • Cyclin-E1
  • E2F2
  • PPARγ
  • Troglitazone
  • Wnt signal

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Komatsu, Y., Ito, I., Wayama, M., Fujimura, A., Akaogi, K., Machida, H., Nakajima, Y., Kuroda, T., Ohmori, K., Murayama, A., Kimura, K., & Yanagisawa, J. (2008). PPARγ ligands suppress the feedback loop between E2F2 and cyclin-E1. Biochemical and Biophysical Research Communications, 370(1), 145-148. https://doi.org/10.1016/j.bbrc.2008.03.046