ArticleNature communications2024
DUSP6 regulates Notch1 signalling in colorectal cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- DUSP4 promotes anti-tumor CD8Nature communications · 2026Article
- DUSP6 promotes motility, invasion, and tumorigenicity of thyroid cancer cells via IL8-induced neutrophil extracellular traps.Scientific reports · 2026Article
- Article
- Dual-specificity phosphatase 6 interferes with the repressive activity of forkhead box O1 towards CYP4A11 that mediates lipid accumulation in the liver.Scientific reports · 2026Article
- Phosphatases in tumor cell immune escape: a perspective based on the camouflage, coercion, cytoprotection.Frontiers in cell and developmental biology · 2026Review
- Effects of the DUSP6 gene on the proliferation and differentiation of porcine subcutaneous preadipocytes.Animal bioscience · 2025Article
- OCT4-mediated upregulation of DUSP6 promotes metastasis in non-small-cell lung cancer.Journal of Cancer · 2025Article
- Progress on the mechanism of intestinal microbiota against colorectal cancer.Frontiers in cellular and infection microbiology · 2025Review
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Authors and funding
14 authors.
Funding
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Abstract
Notch1 plays various roles in cancer development, and Notch1-induced transactivation is controlled by phosphorylation of its cleaved intracellular domain. However, it is unclear whether there are phosphatases capable of dephosphorylating the cleaved Notch1 transmembrane/intracellular region (NTM) to regulate its function. Here, we show that DUSP6 can function as a phosphatase for Notch1, thereby regulating NTM stability and transcriptional activity, thus influencing colorectal cancer (CRC) development. In human CRC cells, elevated DUSP6 expression correlates with increased NTM levels, leading to enhanced CRC cell proliferation both in vitro and in vivo. High tumoral DUSP6 protein expression is associated with poorer overall CRC patient survival. In mice, DUSP6 deficiency results in reduced CRC development. Mechanistically, DUSP6 dephosphorylates phospho-Y2116, which in turn reduces NTM ubiquitination, leading to increased NTM stability and transcriptional activity. As a result, the expression of Notch1-targeted proliferation genes is increased to promote tumour cell growth.
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