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Milena Rizzo [1; 2] and Gabriele Berti [1; 3] and Francesco Russo [4; 5] and Monica Evangelista [1] and Marco Pellegrini [4] and Giuseppe Rainaldi [1; 2]

Academic Editor: Davide Barbagallo

1, Non-coding RNA Laboratory, Institute of Clinical Physiology (IFC), CNR, Via Moruzzi 1, 56124 Pisa, Italy, cnr.it

2, Tuscan Tumor Institute (ITT), Via Alderotti 26/N, 50139 Firenze, Italy, ittumori.it

3, Instute of Life Science, Scuola Superiore Sant’Anna, Piazza Martiri delle Libertà 33, 56127 Pisa, Italy, sssup.it

4, Laboratory of Integrative Systems Medicine (LISM), Institute of Informatics and Telematics (IIT) and Institute of Clinical Physiology (IFC), CNR, Via Moruzzi 1, 56124 Pisa, Italy, cnr.it

5, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark, ku.dk

Received May 30, 2017; Accepted Aug 1, 2017

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.

1. Introduction

It is well known that the deregulation of miRNA expression is one of the causes or contributory causes of cancer development. miRNAs may act as tumor suppressors (TS), oncogenes, or both depending on the tumor context [1]. miR-28-5p is an intragenic miRNA downregulated in several tumor types, such as hepatocellular carcinoma [2], renal cell carcinoma [3], natural killer/T-cell lymphoma [4], B-cell lymphoma [5], colorectal cancer (CRC) [6], and CRC liver metastasis [7, 8], although in some cases, an increased expression level of miR-28-5p has been observed (ovarian, esophageal, and cervical cancer) [9–11]. Most of the papers regarding the role of miR-28-5p in tumors suggested a prevalent tumor suppressor activity of this miRNA in vitro [2, 3, 5, 6, 12]. Very recently, it has been demonstrated that the miR-28-5p reexpression in xenograft models of Burkitt (BL) and diffuse large B-cell lymphoma (DLBCL) as well as in a BL murine model blocked tumor growth, opening the way to miR-28-5p-based replacement therapy as a novel therapeutic strategy for these diseases [13].

The molecular targets through which miR-28-5p exerts its anti- or proproliferative role are only partially known. For example, miR-28-5p reduced cell growth and migration in hepatocellular carcinoma [2] and in CRC [6] cells inhibiting the expression of IGF-1, CCND1, and...

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