Evidence map›Paper›PMID 21908579›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2011

Insulin-like growth factor-binding protein-7 functions as a potential tumor suppressor in hepatocellular carcinoma.

Dong Chen, Byoung Kwon Yoo, Prasanna Kumar Santhekadur, Rachel Gredler, Sujit K Bhutia, Swadesh K Das, Christine Fuller, Zao-zhong Su, Paul B Fisher, Devanand Sarkar

Open access · hybridAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 85 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
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  5. IGF-Binding Protein 7 and Cadmium-Induced Hepatorenal Fibrosis.Journal of the American Society of Nephrology : JASN · 2025
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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

10 authors at 1 institution in 1 country.

Dong ChenDepartment of Pathology, Virginia Commonwealth University, School of Medicine, Richmond, Virginia 23298, USA.
Byoung Kwon Yoo
Prasanna Kumar Santhekadur
Rachel Gredler
Sujit K Bhutia
Swadesh K Das
Christine Fuller
Zao-zhong Su
Paul B Fisher
Devanand Sarkar
Virginia Commonwealth University · US

Funding

Analysis of a novel regulator of hepatocellular carcinomaR01CA138540 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SARKAR, DEVANAND · 2010 to 2014
$1.6M
AEG-1: Novel Gene Involved in Malignant GliomaR01CA134721 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA134721NCI NIH HHS R01 CA138540
6 · The paper itself

Abstract

purposeHepatocellular carcinoma (HCC) is a highly virulent malignancy with no effective treatment, thus requiring innovative and effective targeted therapies. The oncogene astrocyte-elevated gene-1 (AEG-1) plays a seminal role in hepatocarcinogenesis and profoundly downregulates insulin-like growth factor-binding protein-7 (IGFBP7). The present study focuses on analyzing potential tumor suppressor functions of IGFBP7 in HCC and the relevance of IGFBP7 downregulation in mediating AEG-1 function. EXPERIMENTAL

designIGFBP7 expression was detected by immunohistochemistry in HCC tissue microarray and real-time PCR and ELISA in human HCC cell lines. Dual FISH was done to detect LOH at IGFBP7 locus. Stable IGFBP7-overexpressing clones were established in the background of AEG-1-overexpressing human HCC cells and were analyzed for in vitro proliferation and senescence and in vivo tumorigenesis and angiogenesis.

resultsIGFBP7 expression is significantly downregulated in human HCC samples and cell lines compared with normal liver and hepatocytes, respectively, and inversely correlates with the stages and grades of HCC. Genomic deletion of IGFBP7 was identified in 26% of patients with HCC. Forced overexpression of IGFBP7 in AEG-1-overexpressing HCC cells inhibited in vitro growth and induced senescence, and profoundly suppressed in vivo growth in nude mice that might be an end result of inhibition of angiogenesis by IGFBP7.

conclusionThe present findings provide evidence that IGFBP7 functions as a novel putative tumor suppressor for HCC and establish the corollary that IGFBP7 downregulation can effectively modify AEG-1 function. Accordingly, targeted overexpression of IGFBP7 might be a potential novel therapy for HCC.

Indexed as

Genes, Tumor SuppressorAnimalsCarcinoma, HepatocellularCell Adhesion MoleculesCell Line, TumorChick EmbryoChorioallantoic MembraneDown-RegulationHumansImmunohistochemistryInsulin-Like Growth Factor Binding ProteinsLiver NeoplasmsLoss of HeterozygosityMembrane ProteinsMiceMice, NudeCell Adhesion Moleculesinsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsMembrane ProteinsMTDH protein, humanRNA-Binding Proteins

Identifiers

PMID21908579
PMCPMC3207018
OpenAlexW2052728193

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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.