ArticleBMC developmental biology2011
Progenitor expansion in apc mutants is mediated by Jak/Stat signaling.
Article in BMC developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Fraxetin Inhibits the Proliferation and Metastasis of Glioma Cells by Inactivating JAK2/STAT3 Signaling.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Learning complex subcellular distribution patterns of proteins via analysis of immunohistochemistry images.Bioinformatics (Oxford, England) · 2020Article
- A novel group of secretory cells regulates development of the immature intestinal stem cell niche through repression of the main signaling pathways driving proliferation.Developmental biology · 2019Article
- IFN/STAT signaling controls tumorigenesis and the drug response in colorectal cancer.Cancer science · 2019Article
- Canonical Wnt signaling regulates patterning, differentiation and nucleogenesis in mouse hypothalamus and prethalamus.Developmental biology · 2018Article
- Specific immunotherapy in combination with Clostridium butyricum inhibits allergic inflammation in the mouse intestine.Scientific reports · 2015Article
- BCL6 controls Th9 cell development by repressing Il9 transcription.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- MicroRNA-224 suppresses colorectal cancer cell migration by targeting Cdc42.Disease markers · 2014Article
- Elk-1 phosphorylated at threonine-417 is present in diverse cancers and correlates with differentiation grade of colonic adenocarcinoma.Human pathology · 2013Article
- Emergence of zebrafish models in oncology for validating novel anticancer drug targets and nanomaterials.Drug discovery today · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMutations in APC, a negative regulator of the Wnt/ß-catenin pathway, can cause cancer as well as profound developmental defects. In both cases, affected cells adopt a proliferative progenitor state and fail to differentiate. While the upregulation of some target genes of Wnt/ß-catenin signaling has been shown to mediate these phenotypes in individual tissues, it is unclear whether a common mechanism underlies the defects in APC mutants.
resultsHere we show that stat3, a known oncogene and a target of ß-catenin in multiple tissues, is upregulated in apc mutant zebrafish embryos. We further demonstrate that Jak/Stat signaling is necessary for the increased level of proliferation and neural progenitor gene expression observed in apc mutants.
conclusionsTogether, our data suggest that the regulation of Jak/Stat signaling may represent a conserved mechanism explaining the expansion of undifferentiated cells downstream of APC mutations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.