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• W2116624561 abstract "Upregulation of microRNA-21 (miR-21) is known to be strongly associated with the proliferation, invasion, and radio-resistance of glioma cells. However, the regulatory mechanism that governs the biogenesis of miR-21 in glioma is still unclear. Here, we demonstrate that the DEAD-box RNA helicase, DDX23, promotes miR-21 biogenesis at the post-transcriptional level. The expression of DDX23 was enhanced in glioma tissues compared to normal brain, and expression level of DDX23 was highly associated with poor survival of glioma patients. Specific knockdown of DDX23 expression suppressed glioma cell proliferation and invasion in vitro and in vivo, which is similar to the function of miR-21. We found that DDX23 increased the level of miR-21 by promoting primary-to-precursor processing of miR-21 through an interaction with the Drosha microprocessor. Mutagenesis experiments critically demonstrated that the helicase activity of DDX23 was essential for the processing (cropping) of miR-21, and we further found that ivermectin, a RNA helicase inhibitor, decreased miR-21 levels by potentially inhibiting DDX23 activity and blocked invasion and cell proliferation. Moreover, treatment of ivermectin decreased glioma growth in mouse xenografts. Taken together, these results suggest that DDX23 plays an essential role in glioma progression, and might thus be a potential novel target for the therapeutic treatment of glioma. Upregulation of microRNA-21 (miR-21) is strongly associated with glioma malignancy, but the regulatory mechanism that governs miR-21 biogenesis is unclear. Yin et al. demonstrate that the DEAD-box RNA helicase DDX23 promotes miR-21 biogenesis at the post-transcriptional level in glioma cells, and that DDX23 inhibition reduces glioma growth in mouse xenografts." @default.
• W2116624561 created "2016-06-24" @default.
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• W2116624561 date "2015-06-29" @default.
• W2116624561 modified "2023-10-18" @default.
• W2116624561 title "DEAD-box RNA helicase DDX23 modulates glioma malignancy via elevating miR-21 biogenesis" @default.
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• W2116624561 doi "https://doi.org/10.1093/brain/awv167" @default.
• W2116624561 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26121981" @default.
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