Evidence map›Paper›PMID 20357812›Full record

ArticleThe Journal of investigative dermatology2010

Functional modulation of IGF-binding protein-3 expression in melanoma.

Altaf A Dar, Shahana Majid, Mehdi Nosrati, David de Semir, Scot Federman, Mohammed Kashani-Sabet

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Osteonecrosis of the femoral head: genetic basis.International orthopaedics · 2019
    Pooled it
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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 2 institutions in 1 country.

Altaf A DarAuerback Melanoma Research Laboratory, Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California, USA.
Shahana Majid
Mehdi Nosrati
David de Semir
Scot Federman
Mohammed Kashani-Sabet
University of California, San Francisco · USSan Francisco VA Medical Center · US

Funding

Validation of Genomic Targets in MelanomaR01CA114337 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2005 to 2015
$3.2M
Molecular Classification of Primary Cutaneous MelanomaR01CA122947 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2007 to 2011
$1.5M
NCI NIH HHS CA114337NCI NIH HHS CA122947NCI NIH HHS R01 CA114337NCI NIH HHS R01 CA122947
6 · The paper itself

Abstract

IGF-binding protein-3 (IGFBP3) is a member of the IGFBP family, which regulates mitogenic and antiapoptotic effects of IGFs. In this report we evaluated the role of IGFBP3 in melanoma. Quantitative real-time PCR (qRT-PCR), western blot, and ELISA analyses indicated a significant downregulation of IGFBP3 expression in melanoma cell lines as compared with a normal melanocyte cell line. Melanoma cell lines treated with the demethylating agent 5-AZA-2'-deoxycytidine reexpressed IGFBP3 at the mRNA and protein levels. Chromatin immunoprecipitation assays revealed enrichment of acetylated histones H3 and H4, and H3 di- and tri-methylated lysine 4 on the unmethylated IGFBP3 promoter. The IGFBP3 promoter region was highly methylated in human melanoma samples as compared with normal nevi. Overexpression of IGFBP3 in melanoma cells in vitro suppressed tumor cell survival, induced apoptosis, reduced colony formation and invasion, and induced expression of the proapoptotic genes p21, PUMA, and BAX. IGFBP3 overexpression also resulted in cleavage of caspase 3 and reduced expression of phosphorylated AKT. Stable overexpression of IGFBP3 suppressed tumor cell growth in vivo. Our study results indicate that silencing of IGFBP3 in melanoma is due to the methylation of its promoter, and that overexpression of IGFBP3 induces apoptosis and suppresses cell survival and growth.

Indexed as

ApoptosisAzacitidineBase SequenceCaspase 3Cell DivisionCell Line, TumorCell SurvivalChromatinDecitabineDNA MethylationEnzyme InhibitorsGene Expression Regulation, NeoplasticGene SilencingHumansInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor Binding ProteinsAzacitidineCASP3 protein, humanCaspase 3ChromatinDecitabineEnzyme InhibitorsIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor Binding ProteinsRNA, Messenger

Identifiers

PMID20357812
PMCPMC3023991
OpenAlexW1983508324

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.