ArticleThe EMBO journal1996
Growth arrest by the cyclin-dependent kinase inhibitor p27Kip1 is abrogated by c-Myc.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
What it found
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Who cites it
131 citing papers in PubMed, 317 citations in OpenAlex.
- HER3 promotes triple-negative breast cancer progression by upregulating PHF8 via miR-34b-5p-dependent mechanism.Cell death & disease · 2025Article
- Targeting MYC: Multidimensional regulation and therapeutic strategies in oncology.Genes & diseases · 2025Review
- Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025Review
- TLR9 Downregulation in Breast Cancer: Its Role in Tumor Immunity, Inflammatory Response, and Cellular Senescence.Journal of innate immunity · 2025Article
- Connexin 37 sequestering of activated-ERK in the cytoplasm promotes p27-mediated endothelial cell cycle arrest.Life science alliance · 2023Article
- Cell cycle control by the insulin-like growth factor signal: at the crossroad between cell growth and mitotic regulation.Cell cycle (Georgetown, Tex.) · 2023Review
- Co-expression patterns explain how a basic transcriptional role for MYC modulatesCell cycle (Georgetown, Tex.) · 2022Article
- Lyon IARC Polyomavirus Displays Transforming Activities in Primary Human Cells.Journal of virology · 2022Article
- Tumor Suppressive Effects of GAS5 in Cancer Cells.Non-coding RNA · 2022Review
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- Mitogen-activated protein kinase inhibition-induced modulation of epidermal growth factor receptor signaling in human head and neck squamous cell carcinoma.Head & neck · 2021Article
- Myc stimulates cell cycle progression through the activation of Cdk1 and phosphorylation of p27.Scientific reports · 2019Article
- Strategies to generate functionally normal neutrophils to reduce infection and infection-related mortality in cancer chemotherapy.Pharmacology & therapeutics · 2019Review
- Oncogenic MYC amplifies mitotic perturbations.Open biology · 2019Article
- Targeting MYC in multiple myeloma.Leukemia · 2018Review
- BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141.Journal of experimental & clinical cancer research : CR · 2018Article
- Aurora kinases: novel therapy targets in cancers.Oncotarget · 2017Review
- The T-Box factor TBX3 is important in S-phase and is regulated by c-Myc and cyclin A-CDK2.Cell cycle (Georgetown, Tex.) · 2015Article
- Screening of cell cycle fusion proteins to identify kinase signaling networks.Cell cycle (Georgetown, Tex.) · 2015Article
- Eflornithine (DFMO) prevents progression of pancreatic cancer by modulating ornithine decarboxylase signaling.Cancer prevention research (Philadelphia, Pa.) · 2014Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We show here that c-Myc antagonizes the cyclin-dependent kinase (CDK) inhibitor p27Kip1. p27 expressed from recombinant retroviruses in Rat1 cells associated with and inhibited cyclin E/CDK2 complexes, induced accumulation of the pRb and p130 proteins in their hypophosphorylated forms, and arrested cells in G1. Prior expression of c-Myc prevented inactivation of cyclin E/CDK2 as well as dephosphorylation of pRb and p130, and allowed continuous cell proliferation in the presence of p27. This effect did not require ubiquitin-mediated degradation of p27. Myc altered neither the susceptibility of cyclin E/CDK2 to inhibition by p27, nor the intrinsic CDK-inhibitory activity of p27, but induced sequestration of p27 in a form unable to bind cyclin E/CDK2. Neither Myc itself nor other G1-cyclin/CDK complexes were directly responsible for p27 sequestration. Retroviral expression of G1 cyclins (D1-3, E or A) or of the Cdc25A phosphatase did not overcome p27-induced arrest. Growth rescue by Myc required dimerization with Max, DNA binding and an intact transcriptional activation domain, as previously shown for cellular transformation. We propose that this activity is mediated by the product of an as yet unknown Myc-Max target gene(s) and represents an essential aspect of Myc's mitogenic and oncogenic functions.
Indexed as
Identifiers
8978686PMC452484W1481295510What OpenQuestion holds
Registered trials
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.