Evidence map›Paper›PMID 26112163›Full record

ArticleRespiratory research2015

Quantitative analysis of mRNA expression levels and DNA methylation profiles of three neighboring genes: FUS1, NPRL2/G21 and RASSF1A in non-small cell lung cancer patients.

Dorota Pastuszak-Lewandoska, Jacek Kordiak, Monika Migdalska-Sęk, Karolina H Czarnecka, Adam Antczak, Paweł Górski, Ewa Nawrot, Justyna M Kiszałkiewicz, Daria Domańska, Ewa Brzeziańska-Lasota

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

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

  1. Clinical value of combinedOncology reviews · 2026
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  5. Expression ofInternational journal of molecular sciences · 2024
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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.

Dorota Pastuszak-LewandoskaDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. dorota.pastuszak-lewandoska@umed.lodz.pl.
Jacek KordiakDepartment of Chest Surgery, General and Oncological Surgery, University Hospital No. 2, Medical University of Lodz, Lodz, Poland. jacek.kordiak@umed.lodz.pl.
Monika Migdalska-SękDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. monika.migdalska-sek@umed.lodz.pl.
Karolina H CzarneckaDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. karolina.czarnecka@umed.lodz.pl.
Adam AntczakDepartment of General and Oncological Pulmonology, Medical University of Lodz, Lodz, Poland. adam.antczak@umed.lodz.pl.
Paweł GórskiDepartment of Pneumology and Allergology, Medical University of Lodz, Lodz, Poland. pawel.gorski@umed.lodz.pl.
Ewa NawrotDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. ewa.nawrot@umed.lodz.pl.
Justyna M KiszałkiewiczDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. justyna.kiszalkiewicz@gmail.com.
Daria DomańskaDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. daria.domanska@umed.lodz.pl.
Ewa Brzeziańska-LasotaDepartment of Molecular Bases of Medicine, Medical University of Lodz, Pomorska 251, C-5, 92-213, Lodz, Poland. ewa.brzezianska@umed.lodz.pl.
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor suppressor gene (TSG) inactivation plays a crucial role in carcinogenesis. FUS1, NPRL2/G21 and RASSF1A are TSGs from LUCA region at 3p21.3, a critical chromosomal region in lung cancer development. The aim of the study was to analyze and compare the expression levels of these 3 TSGs in NSCLC, as well as in macroscopically unchanged lung tissue surrounding the primary lesion, and to look for the possible epigenetic mechanism of TSG inactivation via gene promoter methylation.

methodsExpression levels of 3 TSGs and 2 DNA methyltransferases, DNMT1 and DNMT3B, were assessed using real-time PCR method (qPCR) in 59 primary non-small cell lung tumors and the matched macroscopically unchanged lung tissue samples. Promoter methylation status of TSGs was analyzed using methylation-specific PCRs (MSP method) and Methylation Index (MI) value was calculated for each gene.

resultsThe expression of all three TSGs were significantly different between NSCLC subtypes: RASSF1A and FUS1 expression levels were significantly lower in squamous cell carcinoma (SCC), and NPRL2/G21 in adenocarcinoma (AC). RASSF1A showed significantly lower expression in tumors vs macroscopically unchanged lung tissues. Methylation frequency was 38-76%, depending on the gene. The highest MI value was found for RASSF1A (52%) and the lowest for NPRL2/G21 (5%). The simultaneous decreased expression and methylation of at least one RASSF1A allele was observed in 71% tumor samples. Inverse correlation between gene expression and promoter methylation was found for FUS1 (rs = -0.41) in SCC subtype. Expression levels of DNMTs were significantly increased in 75-92% NSCLCs and were significantly higher in tumors than in normal lung tissue. However, no correlation between mRNA expression levels of DNMTs and DNA methylation status of the studied TSGs was found.

conclusionsThe results indicate the potential role of the studied TSGs in the differentiation of NSCLC histopathological subtypes. The significant differences in RASSF1A expression levels between NSCLC and macroscopically unchanged lung tissue highlight its possible diagnostic role in lung cancer in situ recognition. High percentage of lung tumor samples with simultaneous RASSF1A decreased expression and gene promoter methylation indicates its epigenetic silencing. However, DNMT overexpression doesn't seem to be a critical determinate of its promoter hypermethylation.

Indexed as

AgedBiomarkers, TumorCarcinoma, Non-Small-Cell LungDEAD-box RNA HelicasesDNA MethylationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiddle AgedReal-Time Polymerase Chain ReactionRNA, MessengerTumor Suppressor ProteinsBiomarkers, TumorDDX1 protein, humanDEAD-box RNA HelicasesNPRL2 protein, humanRASSF1 protein, humanRNA, MessengerTumor Suppressor ProteinsTUSC2 protein, human

Identifiers

PMID26112163
PMCPMC4484633
OpenAlexW1581548422

What OpenQuestion holds

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LicenceCC BY
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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.