Abstract
Non-coding RNAs (ncRNAs), notably microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), have recently gained increasing consideration because of their versatile role as key regulators of gene expression. They adopt diverse mechanisms to regulate transcription and translation, and thereby, the function of the protein, which is associated with several major biological processes. For example, proliferation, differentiation, apoptosis, and metabolic pathways demand fine-tuning for the precise development of a specific tissue or organ. The deregulation of ncRNA expression is concomitant with multiple diseases, including lung diseases. This review highlights recent advances in the post-transcriptional regulation of miRNAs and lncRNAs in lung diseases such as asthma, chronic obstructive pulmonary disease, cystic fibrosis, and idiopathic pulmonary fibrosis. Further, we also discuss the emerging role of ncRNAs as biomarkers as well as therapeutic targets for lung diseases. However, more investigations are required to explore miRNAs and lncRNAs interaction, and their function in the regulation of mRNA expression. Understanding these mechanisms might lead to early diagnosis and the development of novel therapeutics for lung diseases.
Highlights
Non-coding RNAs are non-protein-coding RNA transcripts and were initially believed as “non-functional parts” and/or “junk RNAs” and/or “dark matter” of the human genome
Trafficking (Yamakami et al, 2003; Katoh et al, 2004). These findings suggest miR-126, which directly targets Target of Myb1 (TOM1), represents a crucial role in the regulation of innate immune responses and endosomal trafficking of ubiquitinated proteins in the cystic fibrosis (CF) lung. miR-146a negatively regulates Mucin 5AC (MUC5AC) expression, which is one of the foremost constituents of airway mucus, probably through the c-Jun N-terminal kinase (JNK) and NF-κB signaling in the neutrophil elastase (NE)-induced 16HBE14o-cells (Zhong et al, 2011)
This study indicates that miR-146a dysregulation leads to dysfunctional CF macrophages, which results in impaired host defense and overproduction of inflammatory responses, and contributes to the progression and severity of CF
Summary
Reviewed by: Gopal Pandi, Madurai Kamaraj University, India Giuseppe Biamonti, National Research Council (CNR), Italy
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