ArticleMolecular systems biology2022
Metabolic balance in colorectal cancer is maintained by optimal Wnt signaling levels.
Article in Molecular systems biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Ras-MAPK inhibition induces AXIN1 loss in colorectal cancer by mTOR associated suppression of protein synthesis.Cell communication and signaling : CCS · 2026Article
- Perspectives on cancer therapy-synthetic lethal precision medicine strategies, molecular mechanisms, therapeutic targets and current technical challenges.Cell death discovery · 2025Review
- The HOX Gene Family's Role as Prognostic and Diagnostic Biomarkers in Hematological and Solid Tumors.Cancers · 2025Review
- Integrative multi-omics identification and functional validation of potential targets linking metabolism-immune-colorectal cancer causal pathway.Frontiers in immunology · 2025Article
- Functional proteomics of colon cancer Consensus Molecular Subtypes.British journal of cancer · 2024Article
- Review
- Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.Frontiers in genetics · 2024Review
- Altered lipid metabolism in APC-driven colorectal cancer: the potential for therapeutic intervention.Frontiers in oncology · 2024Review
- Metabolic balance in colorectal cancer is maintained by optimal Wnt signaling levels.Molecular systems biology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt pathways are important for the modulation of tissue homeostasis, and their deregulation is linked to cancer development. Canonical Wnt signaling is hyperactivated in many human colorectal cancers due to genetic alterations of the negative Wnt regulator APC. However, the expression levels of Wnt-dependent targets vary between tumors, and the mechanisms of carcinogenesis concomitant with this Wnt signaling dosage have not been understood. In this study, we integrate whole-genome CRISPR/Cas9 screens with large-scale multi-omic data to delineate functional subtypes of cancer. We engineer APC loss-of-function mutations and thereby hyperactivate Wnt signaling in cells with low endogenous Wnt activity and find that the resulting engineered cells have an unfavorable metabolic equilibrium compared with cells which naturally acquired Wnt hyperactivation. We show that the dosage level of oncogenic Wnt hyperactivation impacts the metabolic equilibrium and the mitochondrial phenotype of a given cell type in a context-dependent manner. These findings illustrate the impact of context-dependent genetic interactions on cellular phenotypes of a central cancer driver mutation and expand our understanding of quantitative modulation of oncogenic signaling in tumorigenesis.
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Registered trials
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