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Analytical Cellular Pathology
Volume 2015 (2015), Article ID 419561, 6 pages
Research Article

Evaluation of the Selenotranscriptome Expression in Two Hepatocellular Carcinoma Cell Lines

1Dipartimento di Biochimica, Biofisica e Patologia Generale, Seconda Università degli Studi di Napoli, 80138 Napoli, Italy
2Dipartimento di Medicina Sperimentale, Seconda Università degli Studi di Napoli, 80138 Napoli, Italy
3Servizio di Informatica Medica, Azienda Ospedaliera Universitaria, Seconda Università di Napoli, 80138 Napoli, Italy
4CROM, Istituto Nazionale Tumori “Fondazione G. Pascale”, IRCCS, 80131 Napoli, Italy

Received 2 April 2015; Accepted 9 June 2015

Academic Editor: José A. Sánchez-Alcázar

Copyright © 2015 Stefano Guariniello et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hepatocellular carcinoma (HCC) is the most common type of liver cancer and is still one of the most fatal cancers. Hence, it needs to identify always new putative markers to improve its diagnosis and prognosis. Since the selenium is able to fight the oxidative damage which is one of the major origins of cell damage as well as cancer, we have recently focused our attention on selenoprotein family and their involvement in HCC. In the present paper we have carried out a global analysis of the selenotranscriptome expression in HepG2 and Huh7 cells compared to the normal human hepatocytes by reverse transcription-qPCR (RT-qPCR). Our data showed that in both cells there are three downregulated (DIO1, DIO2, and SELO) and ten upregulated (GPX4, GPX7, SELK, SELM, SELN, SELT, SELV, SEP15, SEPW1, and TrxR1) genes. Additionally, interactomic studies were carried out to evaluate the ability of these down- and upregulated genes to interact between them as well as to identify putative HUB nodes representing the centers of correlation able to exercise a direct control over the coordinated genes.