Evidence map›Paper›PMID 11244502›Full record

ArticleOncogene2001

Induction of epithelial differentiation and DNA demethylation in hamster malignant oral keratinocyte by ornithine decarboxylase antizyme.

T Tsuji, S Usui, T Aida, T Tachikawa, G F Hu, A Sasaki, T Matsumura, R Todd, D T Wong

Abstract 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Salivary Biomarkers for Oral Cancer Detection: Insights from Human DNA and RNA Analysis.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Review
  5. Review
  6. Review
  7. Article
  8. Extracellular Spermine Activates DNA Methyltransferase 3A and 3B.International journal of molecular sciences · 2019
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  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

9 authors at 4 institutions in 2 countries.

T TsujiDepartment of Oral Medicine and Diagnostic Sciences, Division of Oral Pathology, Harvard School of Dental Medicine, Boston, Massachusetts, MA 02115, USA.
S Usui
T Aida
T Tachikawa
G F Hu
A Sasaki
T Matsumura
R Todd
D T Wong
Showa University · JPBoston University · USHarvard University · USOkayama University · JP

Funding

HPV AND CELL CYCLE DYSREGULATION IN ORAL CANCERP01DE012467 · NIDCR · MASSACHUSETTS GENERAL HOSPITAL · PI WONG, DAVID T · 1998 to 2002
$3.2M
DOC-1 GENE REGULATION IN HUMAN ORAL CANCERR29DE011983 · NIDCR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI TODD, RANDY C. · 1997 to 2001
$108k
ORNITHINE DECARBOXYLASE ANTIZYME (ODC-AZ) IN ORAL CANCERR03DE012529 · NIDCR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI TSUJI, TAKANORI · 1998 to 1999
–
NIDCR NIH HHS DE-11983NIDCR NIH HHS DE-12467NIDCR NIH HHS DE-12529
6 · The paper itself

Abstract

The hamster ornithine decarboxylase antizyme (ODC-Az) cDNA was transfected into the hamster malignant oral keratinocyte cell line, HCPC-1. Ectopic expression of ODC-Az resulted in the reversion of malignant phenotypes and alteration of DNA methylation status of CCGG sites. The phenotypes examined include ODC enzymatic activity, doubling time, morphological change, anchorage dependent growth, tumorigenicity in nude mice, induction of epithelial differentiation marker protein (involucrin), and change of cell cycle position. Comparison of CCGG DNA methylation status of the ODC-Az and control vector transfectants revealed a significant increase in demethylation of 5-methyl cytosines (m5C) of CCGG sites in the ODC-Az transfectants. Ectopic expression of ODC-Az gene in hamster malignant oral keratinocytes led to reduce ODC activity and the subsequent demethylation of 5-methyl cytosines, presumably via the ODC/ polyamines/ decarboxylated S-adenosylmethionine (dc-AdoMet) pathways. Our data suggest that ODC-Az shared the same pathway of polyamines/ dc-AdoMet/DNA methyltransferase (DNA MTase). We propose that ODC-Az mediates a novel mechanism in tumor suppression by DNA demethylation and presumably re-activation of key cellular genes silenced by DNA hypermethylation during cancer development. Oncogene (2001) 20, 24 - 33.

Indexed as

DNA MethylationOrnithine Decarboxylase InhibitorsAgarAnimalsAntineoplastic AgentsBiomarkers, TumorCell CycleCell DifferentiationCell DivisionCricetinaeCulture MediaDecarboxylationDinucleotide RepeatsEnzyme ActivationEpithelial CellsGene Expression ProfilingAgarAntineoplastic AgentsBiomarkers, TumorCulture MediaGrowth InhibitorsOrnithine Decarboxylaseornithine decarboxylase antizymeOrnithine Decarboxylase InhibitorsProteinsS-Adenosylmethionine

Identifiers

PMID11244502
OpenAlexW2002442168

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.