Nemo-like kinase induces apoptosis in DLD-1 human colon cancer cells
Abstract
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.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The effect of mammalian NLK on Wnt signaling depends on cell type: suppressive in 293 and DLD-1, positive in SaOS-2, NB39-nu, and Nh12.
“Thus, the effect of mammalian NLK on Wnt signaling seems to depend on the cell type; NLK plays some suppressive role in Wnt signaling in 29317) and DLD-1 cell lines30) and a positive role in SaOS-2, NB39-nu and Nh12 cell lines (the present study).”
From Mammalian Nemo-like kinase enhances .BETA.-catenin-TCF transcription activity in human osteosarcoma and neuroblastoma cells (2007) · cites this paper as [30]
In colorectal cancer, NLK inhibits cell growth and promotes cell apoptosis via a p53-independent signalling pathway.
“For example, in colorectal cancer, NLK inhibits cell growth and promotes cell apoptosis via a p53-independent signalling pathway [28].”
From Nemo-Like Kinase in Development and Diseases: Insights from Mouse Studies (2020) · cites this paper as [28]
Cites
Ishitani, T., Ninomiya-Tsuji, J., Nagai, S.-I., Nishita, M., Meneghini, M., Barker, N., Waterman, M., Bowerman, B., Clevers, H., Shibuya, H., et al. (1999) · Nature · doi:10.1038/21674 · Cited by 624 · see citing works
Rotation of photoreceptor clusters in the developing drosophila eye requires the nemo gene
Choi, K.-W., & Benzer, S. (1994) · Cell · doi:10.1016/0092-8674(94)90579-7 · Cited by 339 · see citing works
Ishitani, T., Ninomiya-Tsuji, J., & Matsumoto, K. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.4.1379-1389.2003 · Cited by 212 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Cancer survival classification using integrated data sets and intermediate information
Kim, S., Park, T., & Kon, M. (2014) · Artificial Intelligence in Medicine · doi:10.1016/j.artmed.2014.06.003 · Cited by 25 · see citing works
Nemo-Like Kinase in Development and Diseases: Insights from Mouse Studies
Daams, R., & Massoumi, R. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21239203 · Cited by 21 · see citing works
“For example, in colorectal cancer, NLK inhibits cell growth and promotes cell apoptosis via a p53-independent signalling pathway [28].”
BackgroundYASUDA, J., & ICHIKAWA, H. (2007) · Proceedings of the Japan Academy, Series B · doi:10.2183/pjab.83.16 · Cited by 6 · see citing works
Self-citationNemo-like kinase disrupts nuclear import and drives TDP43 mislocalization in ALS
Bekier, M. E., Pinarbasi, E., Krishnan, G., Mesojedec, J. J., Hurley, M., Harikumar Sheela, H., Collins, C. A., Ghaffari, L., de Majo, M., Ullian, E. M., et al. (2025) · Journal of Clinical Investigation · doi:10.1172/jci188138 · Cited by 2 · see citing works
“Among the most consistent and dramatic disease modifiers to emerge from these screens is nemo-like kinase (NLK), a proline-di-rected serine-threonine kinase that regulates cell differentiation, proliferation, and apoptosis (13–15).”
- Authors
- Yasuda, J., Tsuchiya, A., Yamada, T., Sakamoto, M., Sekiya, T., & Hirohashi, S.
- Affiliations
- National Cancer Centre Japan (JP)
- National Cancer Center Research Institute (JP)
- Corresponding author
- Yasuda, Jun
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 308
- Issue
- 2
- Pages
- 227-233
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W1965938332
- Cited by
- 56
- References
- 3
- Citations by year
- 2025: 3 · 2023: 4 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 4 · 2015: 9 · 2014: 4 · 2013: 8 · 2012: 3
- FWCI
- 0.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Health, Labour and Welfare
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- Nemo-like kinase, apoptosis, colon cancer, DLD-1 cells, Wnt/β-catenin signaling, T-cell factor, cell growth inhibition, tumor suppressor, TUNEL
- MeSH terms
- Colonic Neoplasms, Cytoskeletal Proteins, Enzyme Induction, Humans, Mutation, Tumor Cells, Cultured, Signal Transduction, Trans-Activators, Gene Expression, Apoptosis, Protein Serine-Threonine Kinases, Mitogen-Activated Protein Kinases, Intracellular Signaling Peptides and Proteins, beta Catenin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
