Research Papers:

Distinct lncRNA transcriptional fingerprints characterize progressive stages of multiple myeloma

Domenica Ronchetti, Luca Agnelli, Elisa Taiana, Serena Galletti, Martina Manzoni, Katia Todoerti, Pellegrino Musto, Francesco Strozzi and Antonino Neri _

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Oncotarget. 2016; 7:14814-14830. https://doi.org/10.18632/oncotarget.7442

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Domenica Ronchetti1,2,*, Luca Agnelli1,2,*, Elisa Taiana1,2, Serena Galletti1,2, Martina Manzoni1,2, Katia Todoerti3, Pellegrino Musto3, Francesco Strozzi4, Antonino Neri1,2

1Department of Oncology and Hemato-Oncology, University of Milano, Milan, Italy

2Hematology Unit, Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, Milan, Italy

3Laboratory of Pre-Clinical and Translational Research, IRCCS-CROB, Referral Cancer Center of Basilicata, Rionero in Vulture, Potenza, Italy

4Bioinformatics Core Facility, Parco Tecnologico Padano, Lodi, Italy

*These authors have contributed equally to this work

Correspondence to:

Antonino Neri, e-mail: [email protected]

Luca Agnelli, e-mail: [email protected]

Keywords: lncRNA, multiple myeloma, plasma cell dyscrasia, MALAT1, expression profiling

Received: November 02, 2015     Accepted: January 29, 2016     Published: February 17, 2016


Although many efforts have recently contributed to improve our knowledge of molecular pathogenesis of multiple myeloma (MM), the role and significance of long non-coding RNAs (lncRNAs) in plasma cells (PC) malignancies remains virtually absent. To this aim, we developed a custom annotation pipeline of microarray data investigating lncRNA expression in PCs from 20 monoclonal gammopathies of undetermined significance, 33 smoldering MM, 170 MM, and 36 extra-medullary MMs/plasma cell leukemia patients, and 9 healthy donors. Our study identified 31 lncRNAs deregulated in tumor samples compared to normal controls; among these, the upregulation of MALAT1 appeared associated in MM patients with molecular pathways involving cell cycle regulation, p53-mediated DNA damage response, and mRNA maturation processes. Furthermore, we found 21 lncRNAs whose expression were progressively deregulated trough the more aggressive stages of PC dyscrasia, suggesting a possible role in the progression of the disease. Finally, in the context of molecular heterogeneity of MM, we identified a transcriptional fingerprint in hyperdiploid patients, characterized by the upregulation of lncRNAs/pseudogenes related to ribosomal protein genes, known to be upregulated in this molecular group. Overall, the data provides an important resource for future studies on the functions of lncRNAs in the pathology.

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