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A Peptide Nucleic Acid against MicroRNA miR-145-5p Enhances the Expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Calu-3 Cells.
- Source :
-
Molecules (Basel, Switzerland) [Molecules] 2017 Dec 29; Vol. 23 (1). Date of Electronic Publication: 2017 Dec 29. - Publication Year :
- 2017
-
Abstract
- Peptide nucleic acids (PNAs) are very useful tools for gene regulation at different levels, but in particular in the last years their use for targeting microRNA (anti-miR PNAs) has provided impressive advancements. In this respect, microRNAs related to the repression of cystic fibrosis transmembrane conductance regulator (CFTR) gene, which is defective in cystic fibrosis, are of great importance in the development of new type of treatments. In this paper we propose the use of an anti-miR PNA for targeting miR-145, a microRNA reported to suppress CFTR expression. Octaarginine-anti-miR PNA conjugates were delivered to Calu-3 cells, exerting sequence dependent targeting of miR-145-5p. This allowed to enhance expression of the miR-145 regulated CFTR gene, analyzed at mRNA (RT-qPCR, Reverse Transcription quantitative Polymerase Chain Reaction) and CFTR protein (Western blotting) level.<br />Competing Interests: The authors declare no conflict of interest. The founding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.
- Subjects :
- 3' Untranslated Regions genetics
Apoptosis drug effects
Base Sequence
Binding Sites
Cell Line
Cell Proliferation drug effects
Cystic Fibrosis Transmembrane Conductance Regulator genetics
Evolution, Molecular
Humans
MicroRNAs genetics
RNA, Messenger genetics
RNA, Messenger metabolism
Up-Regulation drug effects
Cystic Fibrosis Transmembrane Conductance Regulator metabolism
Gene Expression Regulation drug effects
MicroRNAs metabolism
Peptide Nucleic Acids pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1420-3049
- Volume :
- 23
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Molecules (Basel, Switzerland)
- Publication Type :
- Academic Journal
- Accession number :
- 29286300
- Full Text :
- https://doi.org/10.3390/molecules23010071