Evidence map›Paper›PMID 24469050›Full record

ArticleOncogene2015

Global identification of genes targeted by DNMT3b for epigenetic silencing in lung cancer.

I Teneng, C S Tellez, M A Picchi, D M Klinge, C M Yingling, A M Snider, Y Liu, S A Belinsky

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Targeting Epigenetics in Lung Cancer.Cold Spring Harbor perspectives in medicine · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. DNMT3B Functions: Novel Insights From Human Disease.Frontiers in cell and developmental biology · 2018
    Review
  18. Article
  19. Article
  20. Review
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

8 authors at 1 institution in 1 country.

I TenengLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
C S TellezLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
M A PicchiLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
D M KlingeLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
C M YinglingLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
A M SniderLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
Y LiuLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
S A BelinskyLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
Lovelace Respiratory Research Institute · US

Funding

Genetic and Epigenetic Biomarkers for SCC of the LungR01ES015262 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI BELINSKY, STEVEN A · 2008 to 2012
$3.4M
The Role of de novo Cytosine DNA Methyltransferases 3a & 3b in Gene MethylationF32CA157082 · NCI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TENENG, IVO · 2011 to 2014
$170k
NCI NIH HHS 1F32CA157082NIEHS NIH HHS R01 ES015262
6 · The paper itself

Abstract

The maintenance cytosine DNA methyltransferase DNMT1 and de novo methyltransferase DNMT3b cooperate to establish aberrant DNA methylation and chromatin complexes to repress gene transcription during cancer development. The expression of DNMT3b was constitutively increased 5-20-fold in hTERT/CDK4-immortalized human bronchial epithelial cells (HBECs) before treatment with low doses of tobacco carcinogens. Overexpression of DNMT3b increased and accelerated carcinogen-induced transformation. Genome-wide profiling of transformed HBECs identified 143 DNMT3b-target genes, many of which were transcriptionally regulated by the polycomb repressive complex 2 (PRC2) complex and silenced through aberrant methylation in non-small-cell lung cancer cell lines. Two genes studied in detail, MAL and OLIG2, were silenced during transformation, initially through enrichment for H3K27me3 and H3K9me2, commonly methylated in lung cancer, and exert tumor suppressor effects in vivo through modulating cancer-related pathways. Re-expression of MAL and OLIG2 to physiological levels dramatically reduced the growth of lung tumor xenografts. Our results identify a key role for DNMT3b in the earliest stages of initiation and provide a comprehensive catalog of genes targeted for silencing by this methyltransferase in non-small-cell lung cancer.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCarcinogensChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3BEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansLung NeoplasmsMembrane GlycoproteinsMiceNerve Tissue ProteinsOligodendrocyte Transcription Factor 2Basic Helix-Loop-Helix ProteinsCarcinogensChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BDNMT1 protein, humanDnmt1 protein, mouseMembrane GlycoproteinsNerve Tissue ProteinsOLIG2 protein, humanOligodendrocyte Transcription Factor 2Polycomb Repressive Complex 2Receptors, Interleukin-1TelomeraseTERT protein, humanTIRAP protein, human

Identifiers

PMID24469050
OpenAlexW2015723935

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.