Evidence map›Paper›PMID 11494151›Full record

ArticleOncogene2001

Adhesion-regulated G1 cell cycle arrest in epithelial cells requires the downregulation of c-Myc.

C M Benaud, R B Dickson

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Oncology reports · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Connections between the cell cycle, cell adhesion and the cytoskeleton.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Microenvironmental control of the breast cancer cell cycle.Anatomical record (Hoboken, N.J. : 2007) · 2012
    Review
  14. Article
  15. miRNA profiling along tumour progression in ovarian carcinoma.Journal of cellular and molecular medicine · 2011
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

C M BenaudDepartment of Cell Biology, Vincent T Lombardi Cancer Center, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20007, USA.
R B Dickson
Georgetown University · US

Funding

NIA NIH HHS R01 AG1496
6 · The paper itself

Abstract

Adhesion to the extracellular matrix is required for the expression and activation of the cyclin-cyclin-dependent kinase (CDK) complexes, and for G1 phase progression of non-transformed cells. However, in non-adherent cells no molecular mechanism has yet been proposed for the cell adhesion-dependent up-regulation of the p27 cyclin-dependent kinase inhibitor (CKI), and the associated inhibition of cyclin E-CDK2. We now show that in epithelial cells the expression of c-Myc is tightly regulated by cell-substrate adhesion. When deprived of adhesion, two independently derived mammary epithelial cell lines, 184A1N4 and MCF-10A, rapidly decrease their level of c-Myc mRNA and protein. This decrease in levels of c-Myc correlates with G1 phase arrest, as indicated by hypophosphorylation of pRb and inhibition of the activity of the cyclin E-CDK2 complex. In 184A1N4 cells, cell-substrate adhesion is required for the suppression of p27, and induction of cyclin E, E2F-1, but not cyclins D1 and D3. Enforced expression of c-Myc in non-adherent 184A1N4 and MCF-10A cells reverses the adhesion-dependent inhibition of cell cycle progression. Restoration of c-Myc in non-adherent cells induces the expression of E2F-1, and hyperphosphorylation of pRb in response to EGF treatment. In addition, expression of c-Myc results in the anchorage-independent activation of the CDK2 complex, the associated upregulation of cyclin E, and the destabilization and degradation of p27 by the ubiquitin-proteasome pathway. Our study thus suggests that c-Myc is the link between cell adhesion and the regulation of p27 and cyclin E-CDK2. Furthermore, we describe a role for c-Myc in adhesion-mediated regulation of E2F-1.

Indexed as

CDC2-CDC28 KinasesDNA-Binding ProteinsGenes, mycProto-Oncogene ProteinsTumor Suppressor ProteinsBreastCell AdhesionCell Cycle ProteinsCell LineCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesCyclin ECycloheximideCysteine EndopeptidasesCDC2-CDC28 KinasesCDK2 protein, humanCDK4 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesCyclin ECycloheximideCysteine EndopeptidasesDactinomycinDNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsEpidermal Growth FactorMultienzyme ComplexesNucleic Acid Synthesis InhibitorsProteasome Endopeptidase ComplexProtein Serine-Threonine KinasesProtein Synthesis InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins c-mycRecombinant Fusion ProteinsRetinoblastoma ProteinRNA, MessengerTranscription FactorsTumor Suppressor ProteinsUbiquitins

Identifiers

PMID11494151
OpenAlexW2327590178

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.