Clinical Research Papers:

Dyskerin and TERC expression may condition survival in lung cancer patients

Marianna Penzo, Vienna Ludovini, Davide Trerè, Annamaria Siggillino, Jacopo Vannucci, Guido Bellezza, Lucio Crinò and Lorenzo Montanaro _

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Oncotarget. 2015; 6:21755-21760. https://doi.org/10.18632/oncotarget.4580

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Marianna Penzo1, Vienna Ludovini2, Davide Treré1, Annamaria Siggillino2, Jacopo Vannucci3, Guido Bellezza4, Lucio Crinò2, Lorenzo Montanaro1

1Department of Experimental, Diagnostic and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, I-40138, Italy

2Department of Medical Oncology, S. Maria della Misericordia Hospital, Perugia, I-06156, Italy

3Department of Thoracic Surgery, University of Perugia, Perugia, I-06156, Italy

4Institute of Pathological Anatomy and Histology, University of Perugia, Perugia, I-06156, Italy

Correspondence to:

Lorenzo Montanaro, e-mail: [email protected]

Keywords: lung cancer, dyskerin, TERC, TERC amplification, survival

Received: June 19, 2015     Accepted: July 06, 2015     Published: July 16, 2015


Dyskerin mediates both the modification of uridine on ribosomal and small nuclear RNAs and the stabilization of the telomerase RNA component (TERC). In human tumors dyskerin expression was found to be associated with both rRNA modification and TERC levels. Moreover, dyskerin overexpression has been linked to unfavorable prognosis in a variety of tumor types, however an explanation for the latter association is not available. To clarify this point, we analyzed the connection between dyskerin expression, TERC levels and clinical outcome in two series of primary lung cancers, differing for the presence of TERC gene amplification, a genetic alteration inducing strong TERC overexpression. TERC levels were significantly higher in tumors bearing TERC gene amplification (P = 0.017). In addition, the well-established association between dyskerin expression and TERC levels was observed only in the series without TERC gene amplification (P = 0.003), while it was not present in TERC amplified tumors (P = 0.929). Similarly, the association between dyskerin expression and survival was found in cases not bearing TERC gene amplification (P = 0.009) and was not observed in TERC amplified tumors (P = 0.584). These results indicate that the influence of dyskerin expression on tumor clinical outcome is linked to its role on the maintenance of high levels of TERC.

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