Cholesterol modulation of the expression of mitochondrial aconitase in human prostatic carcinoma cells

Tsui Hsia Feng, Ke Hung Tsui, Horng Heng Juang

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Mitochondrial aconitase (mACON) is the key enzyme for the citrate oxidation in the mitochondrial Krebs cycle. Cholesterol treatment (10 μg/ml of cholesterol and 1 μg/ml of 25-hydroxycholesterol) for 24 h stimulates mACON enzymatic activity in human prostatic carcinoma cells (PC-3) and hepatoma cells (HepG2). Mevastatin, a cholesterol synthesis antagonist, blocked the effect of cholesterol treatment on mACON. The cholesterol treatment stimulated mACON enzymatic activity, which enhanced the citrate utility but decreased intracellular ATP levels in PC-3 cells. The immunoblotting and transient gene expression assays demonstrated that cholesterol treatment enhances the gene expression of mACON. Mutation of the putative sterol response element (SRE) from GACGCCCCACT to GACGCCCATAT abolished the stimulating effects of cholesterol on the promoter activity of mACON gene. The results suggest that cholesterol treatment induces the mACON gene expression through the SRE signal transduction pathway. Our study demonstrated the deregulation of cholesterol on the citrate metabolism.

Original languageEnglish
Pages (from-to)93-100
Number of pages8
JournalChinese Journal of Physiology
Issue number2
Publication statusPublished - Jun 2005
Externally publishedYes


  • ATP
  • Cholesterol
  • Citrate
  • HepG2
  • Mevastatin
  • PC-3
  • Prostate
  • Sterol response element

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Cholesterol modulation of the expression of mitochondrial aconitase in human prostatic carcinoma cells'. Together they form a unique fingerprint.

Cite this