Evidence map›Paper›PMID 15247904›Full record

ArticleOncogene2004

Mechanisms underlying lack of insulin-like growth factor-binding protein-3 expression in non-small-cell lung cancer.

Yoon Soo Chang, Luo Wang, Young-Ah Suh, Li Mao, Saul J Karpen, Fadlo R Khuri, Waun Ki Hong, Ho-Young Lee

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
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  7. Review
  8. Article
  9. Impact of IGF-1, IGF-1R, and IGFBP-3 promoter methylation on the risk and prognosis of esophageal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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 3 institutions in 1 country.

Yoon Soo ChangDepartment of Thoracic Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Box 432, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Luo Wang
Young-Ah Suh
Li Mao
Saul J Karpen
Fadlo R Khuri
Waun Ki Hong
Ho-Young Lee
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USEmory University · US

Funding

MOLECULAR REGULATION OF HEPATIC TRANSPORTERSR01DK056239 · NIDDK · YALE UNIVERSITY · PI KARPEN, SAUL J. · 1999 to 2017
$4.8M
NCI NIH HHS 1R01 CA10081-01A1NIDDK NIH HHS R01 DK056239
6 · The paper itself

Abstract

Expression of insulin-like growth factor-binding protein-3, which (IGFBP-3) inhibits the proliferation of non-small-cell lung cancer (NSCLC) cells by inducing apoptosis, is lost in about half of stage I NSCLC cases. Since promoter methylation can silence gene expression, we investigated whether hypermethylation of the IGFBP-3 promoter is involved in loss of IGFBP-3 expression in NSCLC. We found the IGFBP-3 promoter to be methylated in seven of 13 NSCLC cell lines and in 16 of 23, seven of 9, eight of 11, and six of six tumor specimens from patients with stage I, II, III, and IV NSCLC, respectively. Methylation status correlated with IGFBP-3 mRNA and protein levels in a subset of NSCLC cell lines tested in our study. However, treatment with 5'-aza-2'-deoxycytidine (5'-aza-dC) restored IGFBP-3 expression in four of seven NSCLC cell lines with the methylated promoter, suggesting that multiple mechanisms regulate IGFBP-3 expression in NSCLC. Gel shift and chromatin immunoprecipitation assays showed that methylation of the Sp-1/Sp-3-binding element in the IGFBP-3 promoter influenced the binding of Sp-1, methyl-CpG-binding protein-2 (MeCP2), and histone deacetylase (HDAC). A luciferase construct expressing IGFBP-3 promoter in which the Sp-1/Sp-3 binding element was methylated showed significantly reduced transcriptional activity. The reduction in promoter activity was further suppressed by overexpression of MeCP2, which was rescued by 5'-aza-dC. Thus interference with Sp-1 transactivation by MeCP2 may contribute to the transcriptional defect of IGFBP-3 expression in NSCLC cells with methylated promoter.

Indexed as

Base SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorDNA-Binding ProteinsDNA MethylationDNA, NeoplasmHumansInsulin-Like Growth Factor Binding Protein 3Lung NeoplasmsMolecular Sequence DataPromoter Regions, GeneticSp1 Transcription FactorSp3 Transcription FactorTranscription FactorsDNA-Binding ProteinsDNA, NeoplasmInsulin-Like Growth Factor Binding Protein 3Sp1 Transcription FactorSp3 Transcription FactorTranscription Factors

Identifiers

PMID15247904
OpenAlexW2070965878

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.