Matches in SemOpenAlex for { <https://semopenalex.org/work/W4386409374> ?p ?o ?g. }
- W4386409374 abstract "Neuroblastoma is the most common extracranial solid tumor in childhood and arises from neural crest cells of the developing sympathetic nervous system. Prostaglandin E 2 (PGE 2 ) has been identified as a key pro-inflammatory mediator of the tumor microenvironment (TME) that promotes neuroblastoma progression. We report that the interaction between the microRNA miR-574-5p and CUG-binding protein 1 (CUGBP1) induces the expression of microsomal prostaglandin E 2 synthase 1 (mPGES-1) in neuroblastoma cells, which contributes to PGE 2 biosynthesis. PGE 2 in turn specifically induces the sorting of miR-574-5p into small extracellular vesicles (sEV) in neuroblastoma cell lines. sEV are one of the major players in intercellular communication in the TME. We found that sEV-derived miR-574-5p has a paracrine function in neuroblastoma. It acts as a direct Toll-like receptor 7/8 (TLR7/8) ligand and induces α-smooth muscle actin (α-SMA) expression in fibroblasts, contributing to fibroblast differentiation. This is particularly noteworthy as it has an opposite function to that in the TME of lung carcinoma, another PGE 2 dependent tumor type. Here, sEV-derived miR-574-5p has an autokrine function that inhibits PGE 2 biosynthesis in lung cancer cells. We report that the tetraspanin composition on the surface of sEV is associated with the function of sEV-derived miR-574-5p. This suggests that the vesicles do not only transport miRs, but also appear to influence their mode of action." @default.
- W4386409374 created "2023-09-05" @default.
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- W4386409374 date "2023-09-04" @default.
- W4386409374 modified "2023-10-17" @default.
- W4386409374 title "The multiple functions of miR-574-5p in the neuroblastoma tumor microenvironment" @default.
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- W4386409374 doi "https://doi.org/10.3389/fphar.2023.1183720" @default.
- W4386409374 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37731742" @default.
- W4386409374 hasPublicationYear "2023" @default.
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