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Yasuda, J. et al.

Yasuda, Tsuchiya, Yamada, Sakamoto, Sekiya, Hirohashi,

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

Deregulation of Wnt/beta-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 beta-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/beta-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.[1]

References

Nemo-like kinase induces apoptosis in DLD-1 human colon cancer cells. Yasuda, J., Tsuchiya, A., Yamada, T., Sakamoto, M., Sekiya, T., Hirohashi, S. Biochem. Biophys. Res. Commun. (2003) [Pubmed]

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