Mammalian nemo-like kinase enhances β-catenin-TCF transcription activity in human osteosarcoma and neuroblastoma cells

Jun Yasuda, Hitoshi Ichikawa

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine kinase and has been considered to be a suppressor of Wnt signaling in mammalian cells. Our study, however, has raised the possibility that NLK also functions as a Wnt signaling activator. In human osteosarcoma and neuroblastoma cell lines, NLK specifically enhanced β-catenin-TCF complex transcription activity. The effect required kinase activity of NLK and co-expression of the β-catenin ΔN (constitutive active mutant of β-catenin). The nuclear localization of Lymphoid enhancer factor 1 (LEF1) and β-catenin ΔN was not altered by NLK overexpression regardless of its effect on β-catenin-TCF complex activity. Reporter analysis using LEF1 mutants at known NLK target sites indicated that NLK may have different activation targets for β-catenin-TCF complex. Mutations in the potential NLK phosphorylation sites in β-catenin did not change its transcription activity either. Our results suggest that NLK positively regulates Wnt/β-catenin signaling in a cell type dependent manner through an unidentified mechanism.

Original languageEnglish
Pages (from-to)16-25
Number of pages10
JournalProceedings of the Japan Academy Series B: Physical and Biological Sciences
Volume83
Issue number1
DOIs
Publication statusPublished - 2007

Keywords

  • Nemo-like kinase
  • Neuroblastoma
  • Osteosarcoma
  • TCF
  • Wnt signaling
  • β-catenin

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Physics and Astronomy(all)

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