ArticleProceedings of the National Academy of Sciences of the United States of America2001
Myc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers.
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Who cites it
195 citing papers in PubMed, 425 citations in OpenAlex.
- Redifferentiation of adult human β cells expanded in vitro by inhibition of the WNT pathway.PloS one · 2014Trial
- MAPK-driven MYC/p21 axis controls senescence bypass and BCL-XL dependence in vincristine-resistant rhabdomyosarcoma.iScience · 2026Article
- LARS regulates cellular senescence and autophagy in liver cancer cells.Cell death & disease · 2026Article
- Article
- Acute high-dose irradiation disrupts cell adhesion and Silk-Ovarioid formation in human primary ovarian cells.Journal of ovarian research · 2026Article
- Targeting CPSF73, the mRNA 3' end processing endonuclease, moves cancer cells away from the mesenchymal state.Frontiers in immunology · 2026Article
- ATG7 vs. ATG5: Distinct autophagy pathways shaping TGF-β signaling and endothelial function.PloS one · 2026Article
- The Role of CDKs in the Regulation of the Monocyte/Macrophage Immune Response.Current medicinal chemistry · 2026Review
- DNA methylation protects cancer cells against senescence.Nature communications · 2025Article
- MYC promotes group 3 medulloblastoma cell proliferation and alleviates ROS-induced cell death by upregulating transketolase.Acta neuropathologica communications · 2025Article
- Ursodeoxycholic Acid Exhibits Greater Inhibitory Effects on Cancerous HCT116 Colon Cells than on Noncancerous NCM460 Colon Cells.Nutrients · 2025Article
- Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres.bioRxiv : the preprint server for biology · 2025Article
- Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres.Cells · 2025Article
- Article
- Effect of Diosgenin in Suppressing Viability and Promoting Apoptosis of Human Prostate Cancer Cells: An Interplay with the G Protein-Coupled Oestrogen Receptor?International journal of molecular sciences · 2024Article
- mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema.EMBO reports · 2024Article
- Efficacy of Butyrate to Inhibit Colonic Cancer Cell Growth Is Cell Type-Specific and Apoptosis-Dependent.Nutrients · 2024Article
- HDAC Inhibition Induces CD26 Expression on Multiple Myeloma Cells via the c-Myc/Sp1-mediated Promoter Activation.Cancer research communications · 2024Article
- SUMOylation inhibitor TAK-981 (subasumstat) synergizes with 5-azacytidine in preclinical models of acute myeloid leukemia.Haematologica · 2024Article
- c-Myc inhibits LAPTM5 expression in B-cell lymphomas.Annals of hematology · 2023Article
135 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The cyclin-dependent kinase inhibitor p21((WAF1/CIP1)) inhibits proliferation both in vitro and in vivo, and overexpression of p21 in normal and tumor cell lines results in cell cycle arrest. In contrast, ectopic expression of Myc alleviates G(1) cell cycle arrest. Recent studies showed that Myc can repress p21 transcription, thereby overriding a p21-mediated cell cycle checkpoint. We found that activation of a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen in mouse cells resulted in suppression of endogenous p21 transcription. This effect was observed in the absence of de novo protein synthesis and was independent of histone deacetylase activity. In transient transfection studies, Myc effectively repressed p21 promoter constructs containing only 119 bp of sequence upstream of the transcription start site. This region contains multiple Sp1-binding sites and a potential initiator element, but no canonical Myc DNA-binding sites. Deletion of the potential initiator element does not affect repression of the p21 promoter by c-Myc. Coimmunoprecipitation and glutathione S-transferase pull-down experiments demonstrate that c-Myc may form complexes with Sp1/Sp3. We found that the central region of c-Myc interacts with the zinc finger domain of Sp1. Because Sp1 is required for p21 transcription, it is possible that Myc may down-regulate p21 transcription, at least in part, by sequestering Sp1. Repression of the p21 promoter may contribute to the ability of c-Myc to promote cell proliferation.
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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.