Evidence map›Paper›PMID 20003326›Full record

ArticleMolecular cancer2009

Promoter methylation of IGFBP-3 and p53 expression in ovarian endometrioid carcinoma.

Pao-Ling Torng, Ching-Wei Lin, Michael Wy Chan, Hui-Wen Yang, Su-Cheng Huang, Chin-Tarng Lin

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  13. 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
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  16. Prognostic effect of p53 expression in patients with completely resected colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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 3 institutions in 1 country.

Pao-Ling TorngDepartment of Obstetric and Gynecology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwa. pltorng@ntu.edu.tw
Ching-Wei Lin
Michael Wy Chan
Hui-Wen Yang
Su-Cheng Huang
Chin-Tarng Lin
National Taiwan University Hospital · TWNational Chung Cheng University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth factor binding protein (IGFBP-3) is an antiproliferative, pro-apoptotic and invasion suppressor protein which is transcriptionally regulated by p53. Promoter methylation has been linked to gene silencing and cancer progression. We studied the correlation between IGFBP-3 and p53 expression as well as IGFBP-3 promoter methylation in ovarian endometrioid carcinoma (OEC) by immunohistochemical staining and quantitative methylation-specific PCR (qMSP). Additionally, we assessed the molecular regulatory mechanism of wild type (wt) p53 on IGFBP-3 expression using two subclones of OEC, the OVTW59-P0 (low invasive) and P4 (high invasive) sublines.

resultsIn 60 cases of OEC, 40.0% showed lower IGFBP-3 expression which was significantly correlated with higher IGFBP-3 promoter methylation. p53 overexpression was detected in 35.0% of OEC and was unrelated to clinical outcomes and IGFBP-3. By Kaplan-Meier analysis, patients with lower IGFBP-3, higher IGFBP-3 promoter methylation, and normal p53 were associated most significantly with lower survival rates. In OEC cell line, IGFBP-3 expression was correlated with IGFBP-3 promoter methylation. IGFBP-3 expression was restored after treatment with a DNA methy-transferase inhibitors (5-aza-deoxycytidine) and suppressed by a p53 inhibitor (pifithrin-alpha). The putative p53 regulatory sites on the promoter of IGFBP-3 were identified at -210, -206, -183 and -179 bases upstream of the transcription start site. Directed mutagenesis at these sites quantitatively reduced the transcription activity of IGFBP-3.

conclusionOur data suggests that IGFBP-3 silencing through IGFBP-3 promoter methylation in the absence of p53 overexpression is associated with cancer progression. These results support a potential role of IGFBP-3 methylation in the carcinogenesis of OEC.

Indexed as

DNA MethylationPromoter Regions, GeneticAdultCarcinoma, EndometrioidFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryInsulin-Like Growth Factor Binding Protein 3Middle AgedOvarian NeoplasmsSurvival RateTranscription, GeneticTumor Suppressor Protein p53Insulin-Like Growth Factor Binding Protein 3Tumor Suppressor Protein p53

Identifiers

PMID20003326
PMCPMC2799391
OpenAlexW2130377526

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Registered trials

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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.