KLF2 is downregulated in pancreatic ductal adenocarcinoma and inhibits the growth and migration of cancer cells

Tumour Biol. 2016 Mar;37(3):3425-31. doi: 10.1007/s13277-015-4053-3. Epub 2015 Oct 8.

Abstract

Members of the Kruppel-like factor (KLF) family have been considered as the tumor suppressors for their inhibitory effects on cell proliferation. Dysregulation of KLF2, a member of KLF family, has been observed in various cancer types. However, its expression pattern and functions in the pancreatic ductal adenocarcinoma (PDAC) are unknown. In this study, we examined the expression of KLF2 in PDAC clinical samples and evaluated the functions of KLF2 in the progression of PDAC. KLF2 is shown to be downregulated in PDAC clinical samples and overexpression of KLF2 inhibits the growth, migration, and metastasis of PDAC cancer cells. KLF2 interacts with beta-catenin and negatively regulates the beta-catenin/TCF signaling. Taken together, this study suggests the suppressive functions of KLF2 in PDAC.

Keywords: Beta-catenin/TCF signaling; Cell growth and migration; KLF2; PDAC.

MeSH terms

  • Adenocarcinoma / pathology*
  • Carcinoma, Pancreatic Ductal / pathology*
  • Cell Movement
  • Cell Proliferation
  • HEK293 Cells
  • Humans
  • Kruppel-Like Transcription Factors / analysis
  • Kruppel-Like Transcription Factors / physiology*
  • Neoplasm Metastasis
  • Pancreatic Neoplasms / pathology*
  • Signal Transduction / physiology
  • TCF Transcription Factors / physiology
  • beta Catenin / physiology

Substances

  • CTNNB1 protein, human
  • KLF2 protein, human
  • Kruppel-Like Transcription Factors
  • TCF Transcription Factors
  • beta Catenin