In recent years, with the increase of air pollution, smoking, aging, and respiratory infection, the incidence rate and mortality of lung diseases are increasing annually, which has become a major hazard to human health. N6-methyladenosine (mA) RNA methylation is the most abundant modifications in eukaryotes, and such modified RNA can be specifically recognized and combined by mA recognition proteins and then mediate RNA splicing, maturation, enucleation, degradation, and translation. More and more studies have revealed that the mA modification is involved in the pathogenesis and development of some diseases; however, the mechanisms of mA in lung diseases are poorly understood. In this review, we summarize the latest progress in the biological function of mA modifications in lung diseases and discuss the potential therapeutic and prognostic strategies. The dysregulation of global mA levels and mA regulators may affect the occurrence and development of asthma, chronic obstructive pulmonary disease, lung cancer, and other lung diseases through inflammation and immune function. In lung cancer, this modification has an important impact on malignant cell proliferation, migration, invasion, and drug resistance. In addition, abnormally changed mA-modified proteins in lung cancer tissue samples and circulating tumor cells (CTCs) may be used as diagnostic and prognostic markers of lung cancer. Models composed of multiple mA regulators can be used to evaluate the risk prediction or prognosis of asthma and pulmonary fibrosis. In general, the in-depth study of mA modifications is a frontier direction in disease research. It provides novel insights for understanding of the molecular mechanisms underlying disease occurrence, development, and drug resistance, as well as for the development of effective novel therapeutics.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9679358 | PMC |
http://dx.doi.org/10.1177/15353702221128564 | DOI Listing |
Front Immunol
January 2025
Xin'an Medicine Research Center, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu, China.
Background: is a differentially expressed gene (DEG) between M1 and M2 macrophages. This study explained why it causes opposite effects in different circumstances.
Methods: Gene expression profiles of various cell subsets were compared by mining a public database.
Front Immunol
January 2025
Department of Pathology, Shanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hosipital, Chinese Academy of Medical Sciences/Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, China.
In this article, we report the first case of a 61-year-old woman who was diagnosed with both nodules and cystic lesions in her lungs. The lung nodules were diagnosed as ALK-positive histiocytosis (APH) carrying an gene fusion, which microscopically displayed a mixed morphology of foamy cells, spindle cells, and Touton's giant cells. Immunohistochemistry showed expression of CD163, CD68, and ALK, while fluorescence hybridization (FISH) with second-generation sequencing (NGS) showed the ALK gene fusion with the FLCN gene variant.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Respiratory Department II, National Clinical Research Center for Respiratory Diseases, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Multisystemic smooth muscle dysfunction syndrome (MSMDS) is an autosomal dominant disorder caused by mutations in the gene, resulting in variable clinical manifestation and multi-organ dysfunction. Interstitial lung disease (ILD) is a rare phenotype of this condition. We describe a rare infant case of an 8-month-old boy who presented with progressively worsening dyspnea, along with intermittent episodes of respiratory distress and cyanosis since birth.
View Article and Find Full Text PDFRSC Med Chem
January 2025
Department of Chemistry, The State University of New York at Buffalo Natural Sciences Complex Buffalo NY 14260 USA
Small molecules targeting activating mutations within the epidermal growth factor receptor (EGFR) are efficacious anticancer agents, particularly in non-small cell lung cancer (NSCLC). Among these, lazertinib, a third-generation tyrosine kinase inhibitor (TKI), has recently gained FDA approval for use in combination with amivantamab, a dual EGFR/MET-targeting monoclonal antibody. This review delves into the discovery and development of lazertinib underscoring the improvements in medicinal chemistry properties, especially in comparison with osimertinib.
View Article and Find Full Text PDFJACC Adv
February 2025
Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!