ArticleCancer research2013
MYC acts via the PTEN tumor suppressor to elicit autoregulation and genome-wide gene repression by activation of the Ezh2 methyltransferase.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 82 citations in OpenAlex.
- MYC serine 62 phosphorylation promotes its association with DNA double-strand breaks to facilitate repair and cell survival under genotoxic stress.Genes & development · 2026Article
- ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.Cell communication and signaling : CCS · 2026Article
- Characterization ofInternational journal of molecular sciences · 2025Article
- A germline point mutation in the MYC-FBW7 phosphodegron initiates hematopoietic malignancies.Genes & development · 2024Article
- Antitumor efficacy of a sequence-specific DNA-targeted γPNA-based c-Myc inhibitor.Cell reports. Medicine · 2024Article
- The roles of EZH2 in cancer and its inhibitors.Medical oncology (Northwood, London, England) · 2023Review
- A New Insight into MYC Action: Control of RNA Polymerase II Methylation and Transcription Termination.Biomedicines · 2023Article
- Prolactin promotes crop epithelial proliferation of domestic pigeons (Columba livia) through the Hippo signaling pathway.Journal of animal science · 2023Article
- Regulation of the somatotropic axis by MYC-mediated miRNA repression.Frontiers in cell and developmental biology · 2023Article
- Non-canonical functions of EZH2 in cancer.Frontiers in oncology · 2023Review
- Review
- Isotretinoin and Thalidomide Down-RegulateMolecules (Basel, Switzerland) · 2021Article
- Integrated requirement of non-specific and sequence-specific DNA binding in Myc-driven transcription.The EMBO journal · 2021Article
- Development of cell-based high throughput luminescence assay for drug discovery in inhibiting OCT4/DNA-PKcs and OCT4-MK2 interactions.Biotechnology and bioengineering · 2021Article
- MYC promotes cancer progression by modulating mEMBO reports · 2021Article
- Article
- EZH2-Targeted Therapies in Cancer: Hype or a Reality.Cancer research · 2020Review
- Extracellular vesicle-encapsulated miR-22-3p from bone marrow mesenchymal stem cell promotes osteogenic differentiation via FTO inhibition.Stem cell research & therapy · 2020Article
- Target gene-independent functions of MYC oncoproteins.Nature reviews. Molecular cell biology · 2020Review
- Using antagonistic pleiotropy to design a chemotherapy-induced evolutionary trap to target drug resistance in cancer.Nature genetics · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The control of normal cell growth is a balance between stimulatory and inhibitory signals. MYC is a pleiotropic transcription factor that both activates and represses a broad range of target genes and is indispensable for cell growth. Whereas much is known about gene activation by MYC, there is no established mechanism for the majority of MYC-repressed genes. We report that MYC transcriptionally activates the PTEN tumor suppressor in normal cells to inactivate the phosphoinositide 3-kinase (PI3K) pathway, thus suppressing AKT activation. Suppression of AKT enhances the activity of the EZH2 histone methyltransferase, a subunit of the epigenetic repressor Polycomb Repressive Complex 2 (PRC2), while simultaneously stabilizing the protein. MYC-mediated enhancement in EZH2 protein level and activity results in local and genome-wide elevation in the repressive H3K27me3 histone modification, leading to widespread gene repression including feedback autoregulation of the MYC gene itself. Depletion of either PTEN or EZH2 and inhibition of the PI3K/AKT pathway leads to gene derepression. Importantly, expression of a phospho-defective EZH2 mutant is sufficient to recapitulate nearly half of all MYC-mediated gene repression. We present a novel epigenetic model for MYC-mediated gene repression and propose that PTEN and MYC exist in homeostatic balance to control normal growth, which is disrupted in cancer cells.
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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.