ArticleJournal of cellular physiology2015
p53 Modulates Notch Signaling in MCF-7 Breast Cancer Cells by Associating With the Notch Transcriptional Complex Via MAML1.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Synthesis of novel 11H-indeno[1,2-b]quinoxaline derivatives and their in vitro and in silico insights into anticancer activities.Scientific reports · 2026Article
- Disrupting Notch signalling by a small molecule inhibiting dihydroorotate dehydrogenase activity.Scientific reports · 2026Article
- Combined treatment of Metformin with Frankincense Essential Oil or Manuka Honey Synergistically Inhibited Stemness Characteristics, Enhanced Sensitivity, and Induced Apoptosis in the CD44⁺/CD24Stem cell reviews and reports · 2026Article
- A Missense Variant inInternational journal of molecular sciences · 2024Article
- p53 regulates the effects of DAPT on Rac1 activation and migration of non-small-cell lung cancer cells.Heliyon · 2023Article
- An enhanced triple fluorescence flow-cytometry-based assay shows differential activation of the Notch signaling pathway by human papillomavirus E6 proteins.Scientific reports · 2022Article
- Inhibition of the lncRNA Coded within Transglutaminase 2 Gene Impacts Several Relevant Networks in MCF-7 Breast Cancer Cells.Non-coding RNA · 2021Article
- Article
- A Dynamic Role of Mastermind-Like 1: A Journey Through the Main (Path)ways Between Development and Cancer.Frontiers in cell and developmental biology · 2020Review
- Methylation-mediated silencing of miR-133a-3p promotes breast cancer cell migration and stemness via miR-133a-3p/MAML1/DNMT3A positive feedback loop.Journal of experimental & clinical cancer research : CR · 2019Article
- Exploring Notch Pathway to Elucidate Phenotypic Plasticity and Intra-tumor Heterogeneity in Gliomas.Scientific reports · 2019Article
- Notch signaling pathway regulates CD4Bioscience reports · 2019Article
- CCNG1 (Cyclin G1) regulation by mutant-P53 via induction of Notch3 expression promotes high-grade serous ovarian cancer (HGSOC) tumorigenesis and progression.Cancer medicine · 2019Article
- Notch-1-PTEN-ERK1/2 signaling axis promotes HER2+ breast cancer cell proliferation and stem cell survival.Oncogene · 2018Article
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- Lunatic Fringe and p53 Cooperatively Suppress Mesenchymal Stem-Like Breast Cancer.Neoplasia (New York, N.Y.) · 2017Article
- Article
- Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2.Journal of Cancer · 2016Article
- Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
19 authors at 11 institutions in 3 countries.
Funding
Abstract
p53 and Notch-1 play important roles in breast cancer biology. Notch-1 inhibits p53 activity in cervical and breast cancer cells. Conversely, p53 inhibits Notch activity in T-cells but stimulates it in human keratinocytes. Notch co-activator MAML1 binds p53 and functions as a p53 co-activator. We studied the regulation of Notch signaling by p53 in MCF-7 cells and normal human mammary epithelial cells (HMEC). Results show that overexpression of p53 or activation of endogenous p53 with Nutlin-3 inhibits Notch-dependent transcriptional activity and Notch target expression in a dose-dependent manner. This effect could be partially rescued by transfection of MAML1 but not p300. Standard and quantitative co-immunoprecipitation experiments readily detected a complex containing p53 and Notch-1 in MCF-7 cells. Formation of this complex was inhibited by dominant negative MAML1 (DN-MAML1) and stimulated by wild-type MAML1. Standard and quantitative far-Western experiments showed a complex including p53, Notch-1, and MAML1. Chromatin immunoprecipitation (ChIP) experiments showed that p53 can associate with Notch-dependent HEY1 promoter and this association is inhibited by DN-MAML1 and stimulated by wild-type MAML1. Our data support a model in which p53 associates with the Notch transcriptional complex (NTC) in a MAML1-dependent fashion, most likely through a p53-MAML1 interaction. In our cellular models, the effect of this association is to inhibit Notch-dependent transcription. Our data suggest that p53-null breast cancers may lack this Notch-modulatory mechanism, and that therapeutic strategies that activate wild-type p53 can indirectly cause inhibition of Notch transcriptional activity.
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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.