Differential effects on the miRNome of the treatment of human airway epithelial Calu-3 cells with peptide-nucleic acids (PNAs) targeting microRNAs miR-101-3p and miR-145-5p: Next generation sequencing datasets

Data in Brief

Alessia Finotti¹  Roberto Gambari²  Enrica Fabbri²  Jessica Gasparello² 

[1] Research Center on Innovative Therapy for Cystic Fibrosis, Ferrara University, 44121 Ferrara, Italy;Department of Life Sciences and Biotechnology, Ferrara University, 44121 Ferrara, Italy;

关键词: Peptide nucleic acids;    Cystic fibrosis;    MicroRNAs;    miR-101-3p;    miR-145-5p;    NGS;   

DOI  :  

来源: DOAJ

【 摘 要 】

Since the demonstration that microRNAs are deeply involved in the regulation of Cystic Fibrosis (CF) Transmembrane Conductance Regulator (CFTR) gene, a great attention has been dedicated to possible alteration of the CFTR gene expression by targeting miRNAs causing down-regulation of CFTR and CFTR-associated proteins. The data here presented are related to previously published studies on the effects of treatment of human bronchial cells of PNAs targeting miR-101-3p and miR-145-5p (microRNAs shown to regulate the CFTR mRNA). These data here presented are relative to two companion articles “Treatment of human airway epithelial Calu-3 cells with a Peptide-Nucleic Acid (PNA) targeting the microRNA miR-101-3p is associated with increased expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene” (published in European Journal of Medicinal Chemistry, 2020) and “Peptide Nucleic Acids for MicroRNA Targeting” (published in Methods in Molecular Biology, 2020). The data obtained indicate that, while the expression of most microRNAs is not affected by PNA treatment, some of them are strongly modulated. In particular, some microRNAs involved in CF and/or CFTR regulation are co-inhibited by miR-101-3p and miR-145-5p. Among them, miR-155-5p, miR-125b-5p, miR-132-3p and miR-6873-3p. This has been demonstrated by Next Generation Sequencing (NGS) followed by RT-qPCR and RT-ddPCR validation.

【 授权许可】

Unknown