Evidence map›Paper›PMID 17102589›Full record

ArticleCancer biology & therapy2006

Insulin-like growth factor factor binding protein-2 is a novel mediator of p53 inhibition of insulin-like growth factor signaling.

Adda Grimberg, Carrie M Coleman, Zonggao Shi, Timothy F Burns, Timothy K MacLachlan, Wenge Wang, Wafik S El-Deiry

Open access · greenAbstract read
In one paragraph

Article in Cancer biology & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. IGFBP2-Ceramide Pathway Mediates Divergent Myelin Breakdown in the PNS and CNS Following Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Biological Age, Chronological Age, and Survival in Pulmonary Fibrosis: A Causal Mediation Analysis.American journal of respiratory and critical care medicine · 2024
    Article
  3. Growth Hormone Treatment for Non-GHD Disorders: Excitement Tempered by Biology.The Journal of clinical endocrinology and metabolism · 2024
    Review
  4. Article
  5. Article
  6. FGF1 ameliorates obesity-associated hepatic steatosis by reversing IGFBP2 hypermethylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. IGF-binding protein 2 is a candidate target of therapeutic potential in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  13. Article
  14. Article
  15. Review
  16. IGFBP-2 - taking the lead in growth, metabolism and cancer.Journal of cell communication and signaling · 2015
    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

7 authors at 1 institution in 1 country.

Adda GrimbergDepartment of Pediatrics, University of Pennsylvania School of Medicine, The Children's Hospital of Philadelphia, Pennsylvania 19104-4318, USA. grimberg@email.chop.edu
Carrie M Coleman
Zonggao Shi
Timothy F Burns
Timothy K MacLachlan
Wenge Wang
Wafik S El-Deiry
Children's Hospital of Philadelphia · US

Funding

Role of IGFBP -3 in mediating p53-induced apoptosisK08DK064352 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI GRIMBERG, ADDA · 2002 to 2006
$659k
NIDDK NIH HHS 1 K08 DK64352NIDDK NIH HHS K08 DK064352
6 · The paper itself

Abstract

The p53 tumor suppressor induces cellular growth arrest and apoptosis in response to DNA damage by transcriptionally activating or repressing target genes and also through protein-protein interactions and direct mitochondrial activities. In 1995, insulin-like growth factor binding protein (IGFBP)-3 was identified as one of the genes transcriptionally activated by p53. IGFBP-3 is one of six closely related IGFBP's, with additional IGFBP-related proteins belonging to the IGFBP superfamily. Here we show that IGFBP-2 is also a p53 target. Like IGFBP-3, IGFBP-2 secretion is reduced when p53+/+ lung cancer cells are transfected with human papillomavirus E6, which targets p53 for degradation. IGFBP-2 mRNA is induced by irradiation in vivo in a p53-dependent manner. p53 protein binds IGFBP-2 intronic sequences in an electrophoretic mobility shift assay, and activates transcription in a luciferase assay. Loss of IGFBP-2 inhibits the ability of p53 to inhibit the activation of extracellular signal-regulated kinase (ERK)1 by IGF-I. Thus, p53 effects on the IGF axis are more complex than previously appreciated, and overall transform the axis from IGF-mediated mitogenesis to growth inhibition and apoptosis. This has significant implications for how growth hormone and IGF-I can induce growth without also inducing cancer.

Indexed as

Base SequenceBinding SitesCell DivisionGenes, ReporterHumansInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding ProteinsIntronsLuciferasesModels, GeneticNeoplasmsPhosphorylationSignal TransductionTranscription, GeneticTumor Suppressor Protein p53Insulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding ProteinsLuciferasesTumor Suppressor Protein p53

Identifiers

PMID17102589
PMCPMC1906874
OpenAlexW2049018598

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.