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Expression status of candidate genes in mesothelioma tissues and cell lines

Melaiu, O; Melissari, E; Mutti, L; Bracci, E; De Santi, C; Iofrida, C; Di Russo, M; Cristaudo, A; Bonotti, A; Cipollini, M; Garritano, SI; Foddis, R; Lucchi, M; Pellegrini, S; Gemignani, F; Landi, S

Authors

O Melaiu

E Melissari

L Mutti

E Bracci

C De Santi

C Iofrida

M Di Russo

A Cristaudo

A Bonotti

M Cipollini

SI Garritano

R Foddis

M Lucchi

S Pellegrini

F Gemignani

S Landi



Abstract

In order to broaden knowledge on the pathogenesis of malignant pleural mesothelioma (MPM), we reviewed studies on the MPM-transcriptome and identified 119 deregulated genes. However, there was poor consistency among the studies. Thus, the expression of these genes was further investigated in the present work using reverse transcriptase-quantitative PCR (RT-qPCR) in 15 MPM and 20 non-MPM tissue samples. Fifty-nine genes showed a statistically significant deregulation and were further evaluated in two epithelioid MPM cell lines (compared to MET-5A, a non-MPM cell line). Nine genes (ACSL1, CCNO, CFB, PDGFRB, SULF1, TACC1, THBS2, TIMP3, XPOT) were deregulated with statistical significance in both cell lines, 12 (ASS1, CCNB1, CDH11, COL1A1, CXADR, EIF4G1, GALNT7, ITGA4, KRT5, PTGIS, RAN, SOD1) in at least one cell line, whereas 7 (DSP, HEG1, MCM4, MSLN, NME2, NMU, TNPO2) were close but did not reach the statistical significance in any of the cell line. Patients whose MPM tissues expressed elevated mRNA levels of BIRC5, DSP, NME2, and THBS2 showed a statistically significant shorter overall survival. Although MPM is a poorly studied cancer, some features are starting to emerge. Novel cancer genes are suggested here, in particular those involved in cell–cell and cell–matrix interactions.

Journal Article Type Article
Acceptance Date Nov 4, 2014
Online Publication Date Nov 12, 2014
Publication Date Jan 1, 2015
Deposit Date Oct 26, 2016
Journal Mutation research -Fundamental and Molecular Mechanisms of Mutagenesis
Print ISSN 0027-5107
Publisher Elsevier
Volume 771
Pages 6-12
DOI https://doi.org/10.1016/j.mrfmmm.2014.11.002
Publisher URL http://dx.doi.org/10.1016/j.mrfmmm.2014.11.002
Related Public URLs http://www.sciencedirect.com/science/journal/00275107


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