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KLF10, transforming growth factor-β-inducible early gene 1, acts as a tumor suppressor

  • Ki Duk Song
  • , Duk Jung Kim
  • , Jong Eun Lee
  • , Cheol Heui Yun
  • , Woon Kyu Lee*
  • *Corresponding author for this work
  • Seoul National University
  • The Institute of Hankook Life Science
  • Yonsei University
  • Inha University

Research output: Contribution to journalJournal articlepeer-review

Abstract

Krüppel-like factor 10 (KLF10) has been suggested to be a putative tumor suppressor. In the present study, we generated KLF10 deficient mice to explore this hypothesis in vivo. KLF10 deficient mice exhibited increased predisposition to skin tumorigenesis and markedly accelerated papilloma development after DMBA/TPA treatment. On the other hand, KLF10 deficient keratinocytes showed increased proliferation and apoptosis. In colony formation assays after oncogenic H-Ras transfection, KLF10 deficient mouse embryonic fibroblasts (MEFs) yielded more colonies than wild-type MEFs. Furthermore, KLF10 dose-dependently activated p21WAF1/CIP1 transcription, which was independent of p53 and Sp1 binding sites in p21WAF1/CIP1 promoter. This study demonstrates that KLF10 is a tumor suppressor and that it targets p21WAF1/CIP1 transcription.

Original languageEnglish
Pages (from-to)388-394
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume419
Issue number2
DOIs
StatePublished - 2012.03.9

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • DMBA/TPA
  • Krüppel-like factor 10
  • P21
  • Sp1 binding sites
  • Tumor suppressor

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