ArticleMolecular and cellular biology2008
The activated Notch1 receptor cooperates with alpha-enolase and MBP-1 in modulating c-myc activity.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Glycolysis and glycolytic enzymes in acute myeloid leukemia: Warburg and beyond.Frontiers in pharmacology · 2026Review
- METTL4-mediated nuclear N6-deoxyadenosine methylation promotes metastasis through activating multiple metastasis-inducing targets.Genome biology · 2022Article
- Using bioinformatics approaches to identify survival-related oncomiRs as potential targets of miRNA-based treatments for lung adenocarcinoma.Computational and structural biotechnology journal · 2022Article
- Systematic identification of clinically relevant miRNAs for potential miRNA-based therapy in lung adenocarcinoma.Molecular therapy. Nucleic acids · 2021Article
- Comprehending the crosstalk between Notch, Wnt and Hedgehog signaling pathways in oral squamous cell carcinoma - clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- A high-content screen identifies the vulnerability of MYC-overexpressing cells to dimethylfasudil.PloS one · 2021Article
- Impact of Tissue Enolase 1 Protein Overexpression in Esophageal Cancer Progression.International journal of medical sciences · 2021Article
- Identification and validation of a miRNA-based prognostic signature for cervical cancer through an integrated bioinformatics approach.Scientific reports · 2020Article
- Article
- Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Aggressiveness of Breast Tumors.International journal of molecular sciences · 2019Article
- When Place Matters: Shuttling of Enolase-1 Across Cellular Compartments.Frontiers in cell and developmental biology · 2019Review
- The Biological Significance and Regulatory Mechanism of c-Myc Binding Protein 1 (MBP-1).International journal of molecular sciences · 2018Review
- ER stress-related ATF6 upregulates CIP2A and contributes to poor prognosis of colon cancer.Molecular oncology · 2018Article
- Hidden features: exploring the non-canonical functions of metabolic enzymes.Disease models & mechanisms · 2018Review
- miR‑29a suppresses IL‑13‑induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells.Oncology reports · 2018Article
- Non-canonical functions of enzymes facilitate cross-talk between cell metabolic and regulatory pathways.Experimental & molecular medicine · 2018Review
- Loss of epigenetic regulator TET2 and oncogenic KIT regulate myeloid cell transformation via PI3K pathway.JCI insight · 2018Article
- Small molecule promotes β-catenin citrullination and inhibits Wnt signaling in cancer.Nature chemical biology · 2018Article
- [Role of enolase 1 in hepatocellular carcinoma and possible mechanism].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017Article
- ENOblock, a unique small molecule inhibitor of the non-glycolytic functions of enolase, alleviates the symptoms of type 2 diabetes.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Notch signal pathway plays multifaceted roles to promote or suppress tumorigenesis. The Notch1 receptor intracellular domain (N1IC), the activated form of the Notch1 receptor, activates the c-myc proto-oncogene. The complex of N1IC and transcription factor YY1 binds to the human c-myc promoter to enhance c-myc expression in a CBF1-independent manner. Here we demonstrated that N1IC interacted with the c-Myc-regulating proteins alpha-enolase and c-myc promoter binding protein 1 (MBP-1). Both alpha-enolase and MBP-1 suppressed the N1IC-enhanced activity of the c-myc promoter in a CBF1-independent manner. The YY1 response element in front of the P2 c-myc promoter was essential and sufficient for the modulation of c-myc by N1IC and alpha-enolase or MBP-1. Furthermore, N1IC, YY1, and alpha-enolase or MBP-1 but not CBF1 bound to the c-myc promoter through associating with the YY1 response element. Hemin-induced erythroid differentiation was suppressed by N1IC in K562 cells. This suppression was relieved by the expression of alpha-enolase and MBP-1. In addition, both alpha-enolase and MBP-1 suppressed the N1IC-enhanced colony-forming ability through c-myc. These results indicate that the activated Notch1 receptor and alpha-enolase or MBP-1 cooperate in controlling c-myc expression through binding the YY1 response element of the c-myc promoter to regulate tumorigenesis.
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