New Insights into the Importance of Long Non-Coding RNAs in Lung Cancer: Future Clinical Approaches.

In mammals, a large part of the gene expression products come from the non-coding ribonucleotide sequences of the protein. These short and long sequences are within the range of tens to hundreds of nucleotides, encompassing more than 200 RNA molecules, and their function is known as the molecular structure of long non-coding RNA (lncRNA). LncRNA molecules are unique nucleotides that have a substantial role in epigenetic regulation, transcription, and post-transcriptional modifications in different ways. According to the results of recent studies, lncRNAs have been shown to assume various roles, including tumor suppression or oncogenic functions in common types of cancer such as lung and breast cancer. These non-coding RNAs (ncRNAs) play a pivotal role in activating transcription factors, managing the ribonucleoproteins, the framework for collecting co-proteins, intermittent processing regulations, chromatin status alterations, and maintaining the control within the cell. Cutting-edge technologies have been introduced to disclose several types of lncRNAs within the nucleus and the cytoplasm, which have accomplished important achievements that are applicable in medicine. Due to these efforts, various data centers have been created to facilitate and modify scientific information related to these molecules, including detection, classification, biological evolution, gene status, spatial structure, status, and location of these small molecules. In the present study, we attempt to present the impacts of these ncRNAs on lung cancer with an emphasis on their mechanisms and functions.

PI3K signalling in chronic obstructive pulmonary disease and opportunities for therapy.

Chronic obstructive pulmonary disease (COPD) is a chronic lung disease characterised by airway inflammation and progressive obstruction of the lung airflow. Current pharmacological treatments include bronchodilators, alone or in combination with steroids, or other anti-inflammatory agents, which have only partially contributed to the inhibition of disease progression and mortality. Therefore, further research unravelling the underlying mechanisms is necessary to develop new anti-COPD drugs with both lower toxicity and higher efficacy. Extrinsic signalling pathways play crucial roles in COPD development and exacerbations. In particular, phosphoinositide 3-kinase (PI3K) signalling has recently been shown to be a major driver of the COPD phenotype. Therefore, several small-molecule inhibitors have been identified to block the hyperactivation of this signalling pathway in COPD patients, many of them showing promising outcomes in both preclinical animal models of COPD and human clinical trials. In this review, we discuss the critically important roles played by hyperactivated PI3K signalling in the pathogenesis of COPD. We also critically review current therapeutics based on PI3K inhibition, and provide suggestions focusing on PI3K signalling for the further improvement of the COPD phenotype. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.