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Transcriptional regulation of PCFT by KLF4, HNF4α, CDX2 and C/EBPα: implication in its site-specific expression in

Mai Furumiya1, Katsuhisa Inoue, Kinya Ohta

  • 1Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Nagoya 467-8603, Japan.

Biochemical and Biophysical Research Communications
|January 15, 2013
PubMed

Insights

Transcriptional regulation of the proton-coupled folate transporter (PCFT) involves Krüppel-like factor 4 (KLF4) and hepatocyte nuclear factor 4α (HNF4α). Their interplay with caudal-type homeobox transcription factor 2 (CDX2) and CCAAT/enhancer-binding protein α (C/EBPα) explains PCFT

Area of Science:

  • Molecular Biology
  • Gastroenterology
  • Genetics

Background:

  • The proton-coupled folate transporter (PCFT) is crucial for folate absorption in the small intestine.
  • PCFT exhibits a unique expression pattern, localized primarily to the proximal small intestine.

Purpose of the Study:

  • To investigate the transcriptional regulation of the human PCFT gene.
  • To elucidate the molecular mechanisms underlying PCFT's specific expression profile in the small intestine.

Main Methods:

  • Dual-luciferase reporter assays were performed in human embryonic kidney (HEK) 293 cells.
  • Reporter constructs containing the 5'-flanking sequence of the human PCFT gene were utilized.
  • Western blot analysis was conducted on rat small intestine tissue.

Main Results:

  • Krüppel-like factor 4 (KLF4) significantly enhanced PCFT promoter activity.
  • Hepatocyte nuclear factor 4α (HNF4α) synergistically boosted KLF4-induced activity.
  • Caudal-type homeobox transcription factor 2 (CDX2) and CCAAT/enhancer-binding protein α (C/EBPα) suppressed PCFT promoter activity.
  • Expression patterns of KLF4, HNF4α, CDX2, and C/EBPα in rat intestine correlated with PCFT regulation.

Conclusions:

  • PCFT promoter activity is primarily induced by KLF4.
  • The distinct expression profile of PCFT in the small intestine is likely regulated by the combined actions of HNF4α, CDX2, and C/EBPα.

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