Nemo-like kinase induces apoptosis in DLD-1 human colon cancer cells

Jun Yasuda, Akira Tsuchiya, Tesshi Yamada, Michiie Sakamoto, Takao Sekiya, Setsuo Hirohashi

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Deregulation of Wnt/β-catenin signaling is thought to play a critical role in human carcinogenesis. Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine kinase that suppresses β-catenin/T-cell factor (TCF) complex transcriptional activity through phosphorylation of TCF. Since NLK may be a tumor suppressor as a negative regulator of Wnt/β-catenin pathway, we established tetracycline-inducible NLK and its kinase-negative mutant expression in DLD-1 human colon cancer cells to analyze the effect of NLK on cell growth and viability. The induction of wild-type NLK in DLD-1 cells caused suppression of cell growth whereas the kinase-negative mutant did not. Flow cytometry indicated that NLK expression increased the number of apoptotic cells but did not induce obvious cell cycle arrest. Apoptosis induction by wild-type NLK was confirmed using TUNEL assays. Our results suggest that overexpression of NLK may have targets other than TCF for induction of apoptosis in human colon carcinoma cells.

Original languageEnglish
Pages (from-to)227-233
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume308
Issue number2
DOIs
Publication statusPublished - 2003 Aug 22

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Keywords

  • Apoptosis
  • Colorectal carcinoma
  • NLK
  • TCF
  • β-Catenin

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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