ArticleProceedings of the National Academy of Sciences of the United States of America2000
Overexpression of MYC causes p53-dependent G2 arrest of normal fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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Who cites it
80 citing papers in PubMed, 141 citations in OpenAlex.
- Hepatic gene replacement improves energy metabolism and survival in a mouse model of neonatal mitochondrial disease GRACILE syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Drug Discovery from Gene Expression/Gene Regulation.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Germline-Somatic Interactions in BRCA-Associated Cancers: Unique Molecular Profiles and Clinical Outcomes Linking ATM to TP53 Synthetic Essentiality.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Elucidating the role of EPPK1 in lung adenocarcinoma development.BMC cancer · 2024Article
- A cell competition system with one gene expression from a single-copy gene in one cell.PloS one · 2024Article
- Disruption of the Mammalian Ccr4-Not Complex Contributes to Transcription-Mediated Genome Instability.Cells · 2023Article
- Mitochondrial complex III deficiency drives c-MYC overexpression and illicit cell cycle entry leading to senescence and segmental progeria.Nature communications · 2023Article
- MYC-an emerging player in mitochondrial diseases.Frontiers in cell and developmental biology · 2023Review
- Review
- MYC-Induced Replicative Stress: A Double-Edged Sword for Cancer Development and Treatment.International journal of molecular sciences · 2021Review
- Impairments of Photoreceptor Outer Segments Renewal and Phototransduction Due to a Peripherin Rare Haplotype Variant: Insights from Molecular Modeling.International journal of molecular sciences · 2021Article
- CFP suppresses breast cancer cell growth by TES-mediated upregulation of the transcription factor DDIT3.Oncogene · 2019Article
- Article
- The homeobox transcription factor HB9 induces senescence and blocks differentiation in hematopoietic stem and progenitor cells.Haematologica · 2019Article
- CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth.Haematologica · 2018Article
- xCT (SLC7A11)-mediated metabolic reprogramming promotes non-small cell lung cancer progression.Oncogene · 2018Article
- c-Myc regulates the CDK1/cyclin B1 dependent‑G2/M cell cycle progression by histone H4 acetylation in Raji cells.International journal of molecular medicine · 2018Article
- Co-inhibition of BET proteins and NF-κB as a potential therapy for colorectal cancer through synergistic inhibiting MYC and FOXM1 expressions.Cell death & disease · 2018Article
- Systematic screening of isogenic cancer cells identifies DUSP6 as context-specific synthetic lethal target in melanoma.Oncotarget · 2017Article
- Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of the proto-oncogene MYC has been implicated in the genesis of diverse human cancers. One explanation for the role of MYC in tumorigenesis has been that this gene might drive cells inappropriately through the division cycle, leading to the relentless proliferation characteristic of the neoplastic phenotype. Herein, we report that the overexpression of MYC alone cannot sustain the division cycle of normal cells but instead leads to their arrest in G(2). We used an inducible form of the MYC protein to stimulate normal human and rodent fibroblasts. The stimulated cells passed through G(1) and S but arrested in G(2) and frequently became aneuploid, presumably as a result of inappropriate reinitiation of DNA synthesis. Absence of the tumor suppressor gene p53 or its downstream effector p21 reduced the frequency of both G(2) arrest and aneuploidy, apparently by compromising the G(2) checkpoint control. Thus, relaxation of the G(2) checkpoint may be an essential early event in tumorigenesis by MYC. The loss of p53 function seems to be one mechanism by which this relaxation commonly occurs. These findings dramatize how multiple genetic events can collaborate to produce neoplastic 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.