ArticleCell death & disease2020
Elevated DHODH expression promotes cell proliferation via stabilizing β-catenin in esophageal squamous cell carcinoma.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- The mitochondria-targeting compound PTC299 enhances megakaryocyte and platelet production.Stem cells translational medicine · 2026Article
- Pan-cancer analysis of pyrimidine metabolism reveals signaling pathways connections with chemoresistance role.British journal of cancer · 2026Article
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- Review
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- Fluorescent Isostere (Journal of medicinal chemistry · 2025Article
- Exploring metabolic reprogramming in esophageal cancer: the role of key enzymes in glucose, amino acid, and nucleotide pathways and targeted therapies.Cancer gene therapy · 2025Review
- Mechanisms of S-phase arrest and mitochondrial dysfunction in complex III by DHODH inhibitors in tumorigenic TNBC cells.Histochemistry and cell biology · 2024Article
- Bioinformatics analysis and experimental verification of the cancer-promoting effect of DHODH in clear cell renal cell carcinoma.Scientific reports · 2024Article
- DHODH inhibition represents a therapeutic strategy and improves abiraterone treatment in castration-resistant prostate cancer.Oncogene · 2024Article
- Blocking SLC7A11 attenuates the proliferation of esophageal squamous cell carcinoma cells.Animal cells and systems · 2024Article
- Paired-related homeobox 1 induces epithelial-mesenchymal transition in oesophageal squamous cancer.World journal of gastrointestinal oncology · 2023Article
- Cloning and Characterization of YakAnimals : an open access journal from MDPI · 2023Article
- Dihydroorotate dehydrogenase promotes cell proliferation and suppresses cell death in esophageal squamous cell carcinoma and colorectal carcinoma.Translational cancer research · 2023Article
- Assessment of a novel variation in DHODH gene causing Miller syndrome: The first report in Chinese population.Molecular genetics & genomic medicine · 2023Article
- LY294002 alleviates bone cancer pain by reducing mitochondrial dysfunction and the inflammatory response.International journal of molecular medicine · 2023Article
- Optimization of CRISPR-Cas system for clinical cancer therapy.Bioengineering & translational medicine · 2023Review
- A bioinformatics analysis for diagnostic roles of theJournal of gastrointestinal oncology · 2022Article
- A novel circ_0000654/miR-375/E2F3 ceRNA network in esophageal squamous cell carcinoma.Thoracic cancer · 2022Article
- Drug repositioning for esophageal squamous cell carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a key enzyme in de novo pyrimidine biosynthesis, the expression level of dihydroorotate dehydrogenase (DHODH) has been reported to be elevated in various types of malignant tumors and its tumor-promoting effect was considered to relate to its pyrimidine synthesis function. Here, we revealed one intriguing potential mechanism that DHODH modulated β-catenin signaling in esophageal squamous cell carcinoma (ESCC). We demonstrated that DHODH directly bound to the NH2 terminal of β-catenin, thereby, interrupting the interaction of GSK3β with β-catenin and leading to the abrogation of β-catenin degradation and accumulation of β-catenin in the nucleus, which in turn, resulted in the activation of β-catenin downstream genes, including CCND1, E2F3, Nanog, and OCT4. We further demonstrated that the regulation of β-catenin by DHODH was independent of DHODH catalyzing activity. Univariate and multivariate analyses suggested that DHODH expression might be an independent prognostic factor for ESCC patients. Collectively, our study highlights the pivotal role of DHODH mediated β-catenin signaling and indicates that DHODH may act as a multi-functional switcher from catalyzing pyrimidine metabolism to regulating tumor-related signaling pathways in ESCC.
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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.