Evidence map›Paper›PMID 12101420›Full record

ArticleOncogene2002

The expression of DNA methyltransferases and methyl-CpG-binding proteins is not associated with the methylation status of p14(ARF), p16(INK4a) and RASSF1A in human lung cancer cell lines.

Mitsuo Sato, Yoshitsugu Horio, Yoshitaka Sekido, John D Minna, Kaoru Shimokata, Yoshinori Hasegawa

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. SIRT7 promotes lung cancer progression by destabilizing the tumor suppressor ARF.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Chromosome 16q genesOncology letters · 2016
    Article
  14. Article
  15. Identification of the methylation of p14ARF promoter as a novel non-invasive biomarker for early detection of lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  16. Reduced mRNA expression levels of MBD2 and MBD3 in gastric carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  17. Article
  18. p14ARF promoter region methylation as a marker for gliomas diagnosis.Medical oncology (Northwood, London, England) · 2011
    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

6 authors at 3 institutions in 2 countries.

Mitsuo SatoDepartment of Clinical Preventive Medicine, Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Yoshitsugu Horio
Yoshitaka Sekido
John D Minna
Kaoru Shimokata
Yoshinori Hasegawa
Showa University · JPNagoya University · JPThe University of Texas Southwestern Medical Center · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
HUMAN 3P RECESSIVE ONCOGENESR01CA071618 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MINNA, JOHN D · 1996 to 2004
$1.4M
NCI NIH HHS CA71618NCI NIH HHS P50 CA70907
6 · The paper itself

Abstract

Promoter hypermethylation is an important means for the transcriptional repression of a number of cancer-associated genes. However, the underlying mechanism of this aberration in cancer remains unclear. Here, we examined 5' CpG island methylation status and expression of the p14(ARF), p16(INK4a) and RASSF1A tumor suppressor genes, and investigated the relationship of these factors with the mRNA expression of DNA methyltransferases (DNMTs) and/or methyl-CpG-binding proteins (MBPs) in 30 lung cancer cell lines including 12 small cell lung cancers (SCLCs) and 18 non-small cell lung cancers (NSCLCs). When beta-actin was used as an internal control, the mRNA expression of three DNMTs (DNMT1, DNMT3A, and DNMT3B) and five MBPs (MBD1, MBD2, MBD3, MBD4, and MeCP2) was upregulated in SCLC, while only that of DNMT1, DNMT3B and MBD3 was upregulated in NSCLC, compared with normal lung tissues. However, when normalized using proliferating cell nuclear antigen (PCNA) as an internal control, these differences disappeared or diminished; there was even a significant reduction in the expression ratios of DNMT1, MBD2 and MeCP2 in SCLC and DNMT1, MBD2 and MBD4 in NSCLC. Furthermore, although significant correlations between PCNA expression and mRNA expression levels of the three DNMTs and four of the MBPs (excluding MeCP2) were observed, there was no obvious correlation between promoter hypermethylation of these tumor suppressor genes and the expression level of any of the DNMTs or MBPs. Our results suggest that upregulation of DNMTs and MBPs probably reflects an increased cell proliferation in human lung cancers and that there are likely to exist gene-specific mechanisms for epigenetic gene silencing.

Indexed as

CpG IslandsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorTumor Suppressor ProteinsCarcinoma, Non-Small-Cell LungCarcinoma, Small CellCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsDNA MethylationDNA Modification MethylasesDNA, NeoplasmGene DeletionHumansLung NeoplasmsNeoplasm ProteinsPromoter Regions, GeneticCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsDNA Modification MethylasesDNA, NeoplasmNeoplasm ProteinsRASSF1 protein, humanRNA, NeoplasmTumor Suppressor Protein p14ARFTumor Suppressor Proteins

Identifiers

PMID12101420
OpenAlexW2053468229

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.