Differential expression profiling of long non-coding RNA GAS5 and miR-126-3p in human cancer cells in response to sorafenib.

Long non-coding RNAs (lncRNAs) and microRNAs are involved in numerous physio-pathological conditions included cancer. To better understand the molecular mechanism of the oral antitumor multikinase inhibitor sorafenib, we profiled the expression of a panel of lncRNAs and miRNAs by qPCR array in a sorafenib-treated hepatocellular carcinoma (HCC) cell line. Among the most affected ncRNAs, we found that sorafenib mediated the dysregulation of the lncRNAs GAS5, HOTTIP and HOXA-AS2 and the miR-126-3p, in a panel of human cancer cell lines (HCC, renal and breast carcinomas). By luciferase gene reporter assay, we discovered that GAS5 may act as a sponge for miR-126-3p in HCC cells. The expression level of GAS5 and miR-126-3p was verified in human liquid and/or solid biopsies from HCC patients. miR-126-3p expression in HCC tissues was decreased respect to their correspondent peritumoral tissues. The levels of plasmatic circulating miR-126-3p and GAS5 were significantly higher and lower in HCC patients compared to healthy subjects, respectively. This study highlighted the capability of sorafenib to modulate the expression of a wide range of ncRNAs and specifically, GAS5 and miR-126-3p were involved in the response to sorafenib of different cancer cell types.

[Corrigendum] Analysis of a nanoparticle­enriched fraction of plasma reveals miRNA candidates for Down syndrome pathogenesis.

After the publication of the above paper, the authors noted that the names of a couple of the authors listed on the paper were associated with the wrong affliation: Specifically, the eighth and ninth listed authors, Francesca Antonaros and Allison Piovesan, are located at DIMES at the University of Florence (fourth affiliation address), not at CSGI, the Research Center for Colloids and Nanoscience in Florence (third affliation address). Therefore, the author and affiliation details for this paper should have been presented as follows: ALESSANDRO SALVI1, MARIKA VEZZOLI2, SARA BUSATTO1, LUCIA PAOLINI1,3, TERESA FARANDA1, EDOARDO ABENI1, MARIA CARACAUSI4, FRANCESCA ANTONAROS4, ALLISON PIOVESAN4, CHIARA LOCATELLI5, GUIDO COCCHI5,6, GUALTIERO ALVISI7, GIUSEPPINA DE PETRO1, DORIS RICOTTA1, PAOLO BERGESE1,3 and ANNALISA RADEGHIERI1,3. 1Department of Molecular and Translational Medicine, University of Brescia; 2Unit of Biostatistics, Department of Molecular and Translational Medicine, University of Brescia, I­25123 Brescia; 3CSGI, Research Center for Colloids and Nanoscience, Sesto Fiorentino, I­50019 Florence; 4Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna; 5Neonatology Unit, St. Orsola­Malpighi Polyclinic; 6Department of Medical and Surgical Sciences (DIMEC), University of Bologna, I­40138 Bologna; 7Department of Molecular Medicine, University of Padua, I­35121 Padua, Italy. The authors regret that this error with the author affiliations for Francesca Antonaros and Allison Piovesan was not noticed prior to the publication of their paper, and apologize for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 43: 2303­2318, 2018; DOI: 10.3892/ijmm.2019.4158].

Analysis of a nanoparticle­enriched fraction of plasma reveals miRNA candidates for Down syndrome pathogenesis.

Down syndrome (DS) is caused by the presence of part or all of a third copy of chromosome 21. DS is associated with several phenotypes, including intellectual disability, congenital heart disease, childhood leukemia and immune defects. Specific microRNAs (miRNAs/miR) have been described to be associated with DS, although none of them so far have been unequivocally linked to the pathology. The present study focuses to the best of our knowledge for the first time on the miRNAs contained in nanosized RNA carriers circulating in the blood. Fractions enriched in nanosized RNA­carriers were separated from the plasma of young participants with DS and their non­trisomic siblings and miRNAs were extracted. A microarray­based analysis on a small cohort of samples led to the identification of the three most abundant miRNAs, namely miR­16­5p, miR­99b­5p and miR­144­3p. These miRNAs were then profiled for 15 pairs of DS and non­trisomic sibling couples by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). Results identified a clear differential expression trend of these miRNAs in DS with respect to their non­trisomic siblings and gene ontology analysis pointed to their potential role in a number of typical DS features, including 'nervous system development', 'neuronal cell body' and certain forms of 'leukemia'. Finally, these expression levels were associated with certain typical quantitative and qualitative clinical features of DS. These results contribute to the efforts in defining the DS­associated pathogenic mechanisms and emphasize the importance of properly stratifying the miRNA fluid vehicles in order to probe biomolecules that are otherwise hidden and/or not accessible to (standard) analysis.