Evidence map›Paper›PMID 25254143›Full record

ArticleJournal of cancer therapy2014

Activation of various downstream signaling molecules by IGFBP-3.

Hanief Mohammad Shahjee, Nisan Bhattacharyya

Open access · diamondAbstract read
In one paragraph

Article in Journal of cancer therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Dynamics of m6A RNA Methylome on the Hallmarks of Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. The Correlation between Body Mass Index with the Occurrence of Skin Tag.Open access Macedonian journal of medical sciences · 2017
    Article
  13. Article
  14. Article
  15. Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting.Journal of experimental & clinical cancer research : CR · 2016
    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

2 authors at 1 institution in 1 country.

Hanief Mohammad ShahjeeDiabetes Branch, NIDDK, National Institutes of Health, Bldg 10-Room 8D12, 9000 Rockville Pike, MSC 1758, Bethesda, MD 20892, United States.
Nisan BhattacharyyaDiabetes Branch, NIDDK, National Institutes of Health, Bldg 10-Room 8D12, 9000 Rockville Pike, MSC 1758, Bethesda, MD 20892, United States.
National Institutes of Health · US

Funding

Induction of Human Prostate Cancer Cell Apoptosis by an IGFBP-3 FragmentZ01DK055121 · NIDDK · DIABETES, DIGESTIVE, KIDNEY DISEASES · PI RECHLER, MATTHEW M · 2007 to 2007
$323k
Intramural NIH HHS Z01 DK055121
6 · The paper itself

Abstract

Insulin-like growth factor binding protein-3 (IGFBP-3), a secretory protein, is the most abundant IGF binding protein present in human serum among all IGF binding proteins. IGFBP-3 shows decreased level of expression in cancerous cells but has been known to be present in significant amounts in normal or non-cancerous cells. IGFBP-3 can induce apoptosis in prostate cancer cells either in an IGF-dependent manner or independently of IGF binding. Although putative cell death specific Insulin-like growth factor binding protein-3 (IGFBP-3R) receptor(s) has recently been identified by which IGFBP-3 may induce its anti-tumor effects, IGFBP-3 has also been known to activate various downstream intracellular signaling molecules via a different mechanistic pathway. Stat-1 has been known to be one of the candidate molecules activated by IGFBP-3. IGFBP-3 can also inhibit Akt/IGF-1 survival pathway in MCF- 7 breast cancer cells which ultimately leads to the induction of apoptosis in these cells. All these studies clearly demonstrate that IGFBP-3 regulates cell proliferation and promotes its pro-apoptotic effects in cancer cells in two different pathways,1) sequester IGF-I to bind to IGF-I receptor to inhibit cell proliferation and induce apoptosis, 2) independent of IGF-I pathway, IGFBP-3 binds to some putative receptor and activate various downstream pro-apoptotic molecules involved in cell death.

Indexed as

ApoptosisIGFBP-3IGF-IStat-1TGF-β

Identifiers

PMID25254143
PMCPMC4170070
OpenAlexW1984655291

What OpenQuestion holds

Textmetadata
LicenceTDM
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.