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Regulation of KLF5 involves the Sp1 transcription factor in human epithelial cells

Ceshi Chen1, Yingfa Zhou, Zhongmei Zhou

  • 1Department of Oncology and Hematology, Winship Cancer Institute, Emory University School of Medicine, 1365-C Clifton Road, Atlanta, GA 30322, USA.

Gene
|April 17, 2004
PubMed

Insights

Human Kruppel-like factor 5 (KLF5) acts as a tumor suppressor, but its expression is often lost in cancers. This study identifies Sp1 as a key transcription factor regulating KLF5, crucial for its dynamic expression in cancer cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Human Kruppel-like factor 5 (hKLF5) is a transcription factor implicated in tumor suppression in prostate and breast cancers.
  • Reduced hKLF5 expression is frequently observed in cancer samples, with mechanisms beyond hemizygous deletion and promoter methylation remaining unclear.

Purpose of the Study:

  • To investigate the transcriptional regulation of the hKLF5 gene.
  • To identify key cis-elements and transcription factors involved in hKLF5 gene expression.

Main Methods:

  • Cloning and functional characterization of the hKLF5 5'-flanking region.
  • Deletion mapping and promoter activity assays in epithelial cell lines.
  • Electrophoretic mobility shift assays (EMSAs) and Sp1 overexpression studies.

Main Results:

  • The hKLF5 promoter lacks a TATA box and is GC-rich, with multiple cis-elements influencing transcription.
  • An Sp1 binding site between -239 and -219 is essential for basal promoter activity.
  • Sp1 protein binds to this site and overexpression of Sp1 transactivates hKLF5 promoter activity.

Conclusions:

  • Sp1 is identified as a critical transcription factor mediating the dynamic transcriptional regulation of hKLF5.
  • Understanding KLF5 regulation by Sp1 offers insights into its potential tumor suppressor role and therapeutic targeting in cancer.

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