ArticleMolecular and cellular biology2014
The myc 3' wnt-responsive element suppresses colonic tumorigenesis.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Tristetraprolin targets Nos2 expression in the colonic epithelium.Scientific reports · 2019Article
- Increased Musashi-2 and Decreased NUMB Protein Levels Observed in Human Colorectal Cancer are reverted to Normal Levels by ATRA-Induced Cell Differentiation.International journal of cancer research & therapy · 2018Article
- The MYC 3' Wnt-Responsive Element Drives Oncogenic MYC Expression in Human Colorectal Cancer Cells.Cancers · 2016Article
- A Role for MYC in Lithium-Stimulated Repair of the Colonic Epithelium After DSS-Induced Damage in Mice.Digestive diseases and sciences · 2016Article
- Regenerating Reputations: Are Wnt and Myc the Good Guys After All?Digestive diseases and sciences · 2016Article
- Regulation of MYC gene expression by aberrant Wnt/β-catenin signaling in colorectal cancer.World journal of biological chemistry · 2015Review
- Inferring regulatory element landscapes and transcription factor networks from cancer methylomes.Genome biology · 2015Article
- A dynamic exchange of TCF3 and TCF4 transcription factors controls MYC expression in colorectal cancer cells.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in components of the Wnt/β-catenin signaling pathway are commonly found in colorectal cancers, and these mutations cause aberrant expression of genes controlled by Wnt-responsive DNA elements (WREs). While the c-Myc proto-oncogene (Myc) is required for intestinal phenotypes associated with pathogenic Wnt/β-catenin signaling in vivo, the WREs that control Myc expression in this setting have yet to be fully described. Previously, we demonstrated that the Myc 3' WRE was required for intestinal homeostasis and intestinal repair in response to damage. Here, we tested the role of the Myc 3' WRE in intestinal tumorigenesis using two independent mouse models. In comparison to Apc(Min/+) mice, Apc(Min/+) Myc 3' WRE(-/-) mice contained 25% fewer tumors in the small intestine. Deletion of the Myc 3' WRE(-/-) in the Apc(Min/+) background resulted in 4-fold more colonic tumors. In a model of colitis-associated colorectal cancer, the Myc 3' WRE suppressed colonic tumorigenesis, most notably within the cecum. Using chromatin immunoprecipitation and transcript analysis of purified colonic crypts, we found that the Myc 3' WRE is required for the transcriptional regulation of Myc expression in vivo. These results emphasize the critical role of the Myc 3' WRE in maintaining homeostatic Myc expression.
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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.