Cancer-derived exosomal miR-138-5p modulates polarization of tumor-associated macrophages through inhibition of KDM6B.

Differential activation of macrophages correlates closely with tumor progression, and the epigenetic factor lysine demethylase 6B (KDM6B, previously named JMJD3) mediates the regulation of macrophage polarization through an unknown mechanism. We developed a suspension coculture system comprising breast cancer cells and macrophages and used RT-qPCR and western blotting to measure expression. Bioinformatics and luciferase reporter assays were used to identify candidate microRNAs of cancer cells responsible for the downregulation of KDM6B.

miR-496/MMP10 Is Involved in the Proliferation of IL-1β-Induced Fibroblast-Like Synoviocytes Via Mediating the NF-κB Signaling Pathway.

Rheumatoid arthritis (RA) is a common chronic autoimmune disease featured by synovial inflammation. miR-496 is closely involved in various pathologic conditions. However, its role in RA has not yet been elucidated.

Detection of Microaneurysms in Fundus Images Based on an Attention Mechanism.

Microaneurysms (MAs) are the earliest detectable diabetic retinopathy (DR) lesions. Thus, the ability to automatically detect MAs is critical for the early diagnosis of DR. However, achieving the accurate and reliable detection of MAs remains a significant challenge due to the size and complexity of retinal fundus images.

Skipping of an exon with a nonsense mutation in the DMD gene is induced by the conversion of a splicing enhancer to a splicing silencer.

Modulation of dystrophin pre-mRNA splicing is an attractive strategy to ameliorate the severe phenotype of Duchenne muscular dystrophy (DMD), although this requires a better understanding of the mechanism of splicing regulation. Aberrant splicing caused by gene mutations provides a good model to study splicing regulatory cis-elements and binding proteins. In this study, we identified skipping of in-frame exon 25 induced by a nonsense mutation (NM_004006.