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Tumor suppressor activity of KLF6 mediated by downregulation of the PTTG1 oncogene

Ursula E Lee1, Zahra Ghiassi-Nejad, Andrew J Paris

  • 1Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

FEBS Letters
|February 2, 2010
PubMed

Insights

The tumor suppressor Kruppel-like factor 6 (KLF6) normally inhibits hepatocellular carcinoma (HCC) growth. Its inactivation leads to increased oncogene PTTG1, promoting tumor development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hepatocellular carcinoma (HCC) frequently involves the inactivation of the Kruppel-like factor 6 (KLF6) tumor suppressor.
  • Understanding KLF6's downstream targets is crucial for elucidating its role in HCC pathogenesis.

Purpose of the Study:

  • To identify downstream transcriptional targets of KLF6.
  • To investigate the relationship between KLF6 and Pituitary tumor transforming gene 1 (PTTG1) in HCC.

Main Methods:

  • Comparative cDNA microarray analysis of liver tissue from KLF6+/+ and KLF6+/- mice.
  • Quantitative analysis of KLF6 and PTTG1 mRNA levels in human HCC samples.
  • In vitro studies using HepG2 cells to assess KLF6's effect on PTTG1 expression and cell proliferation via siRNA.

Main Results:

  • PTTG1 was identified as a key up-regulated transcript in KLF6+/- mouse liver.
  • Decreased KLF6 mRNA correlated with increased PTTG1 in human HCCs.
  • KLF6 directly repressed PTTG1 transcription in HepG2 cells, and KLF6 downregulation promoted proliferation, while PTTG1 downregulation inhibited it.

Conclusions:

  • KLF6 directly represses the oncogene PTTG1, acting as a tumor suppressor in HCC.
  • PTTG1 downregulation represents a novel tumor suppressor pathway mediated by KLF6.

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