Asthma is a chronic inflammatory disturbance of the airways in which many cells and cellular elements are involved. Wheezing, breathlessness, chest tightness, and coughing, especially at night or in the early morning, are typical symptoms of asthma. At present, inhaled corticosteroid (ICS) and long-acting β-agonists (LABAs) are standard treatments for regular management. Oral corticosteroids (OCSs) were recommended for controlling asthma exacerbation but only for a short-term treatment because of the side effects on organs. Biologic therapies have achieved exciting and notable effects in clinical treatment but are not applicable for all phenotypes of asthma. At present, some new approaches are under exploration to lessen side effects and improve curative effects. Studies have revealed that bone marrow mesenchymal stem cells (BMMSCs) hold various curative effects in asthma and may benefit in the long term with high safety. Extracellular vesicles (EVs) enriched in body fluid were characterized as subcomponents of extracellular vesicles and delivered carriers combined with genetic messages in vivo. The therapeutic potential of exosomes has become a research hotspot in many diseases. BMMSC-derived exosomes were considered as the dominant part of BMMSCs in cell-to-cell communications and playing curative effects. Points also hold that BMMSC-Exo could interfere with airway inflammation and airway remolding in asthma via modulating the immune response, regulating gene expression, adjusting the phenotype of macrophage, etc. However, BMMSC-Exo still lacked more clinical trials for evaluating the effects on asthma, and the technology of extraction and purification still needs to be improved for wide use. This review aims to draw the relationship among asthma, BMMSC, and exosome, which may provide innovate ideas for treatment of asthma, and arouse attention about the curative potential of BMMSC-Exo.

Background: Recent findings underscore the importance of ribosome biogenesis, a complex molecular machinery, in cancer biology, highlighting opportunities for targeted treatment strategies. Here, we revealed that dysregulation of ribosome biogenesis is a distinctive feature of non-small lung cancer (NSCLC). However, further investigation is required to pinpoint which specific processes within this complex pathway are aberrant in this malignancy. Methods: The expression levels and clinical significance of NOP56 in NSCLC were investigated by microarray analysis, qPCR, TCGA and GEO datasets. Function assays were conducted to explore the biological role of NOP56 in NSCLC cells. The mechanisms that mediate the upregulation of NOP56 were investigated by bisulfite DNA sequencing, luciferase reporter assay, chromatin immunoprecipitation and TCGA datasets. The downstream pathway of NOP56 was explored by RNA sequencing, qPCR, Western blot and luciferase reporter assay. Results: High expression of NOP56 was detected in NSCLC tissues and was associated with poor prognosis. Functional assays revealed that overexpression of NOP56 promoted NSCLC cellular proliferation, metastasis and ribosome biogenesis in vitro, and further accelerated tumorigenesis in vivo. Mechanistically, NOP56 activates MYC signaling by regulating IRES-dependent translation, which in turn transcriptionally upregulated NOP56 expression, creating a positive feedback loop. Additionally, hypomethylation also contributed to the upregulation of NOP56 in NSCLC. Conclusions: Our study demonstrated that NOP56/MYC forms a positive feedback loop that enhances ribosome biogenesis and drives the progression of NSLSC, positioning NOP56 a promising therapeutic target for this malignancy.