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• W4313374745 endingPage "91.10" @default.
• W4313374745 startingPage "91.10" @default.
• W4313374745 abstract "Abstract Daratumumab is the first CD38 antibody drug for MM patients therapy. CD38 remains at a low level during daratumumab treatment and shows a sustained high quality response. In daratumumab resistant MM cells, CD38 expression was found either totally restored or at even higher levels. Nevertheless, a strategy to pressure the MM cells to maintain low CD-38 expression may have clinical benefit. miR-26a is usually downregulated in cancer and has been show to have potential clinical use. Here, we investigated miR-26a function in MM and tested single-wall carbon nanotube delivery of miR-26a in vitro and in vivo. GSE16558 dataset analysis showed miR-26a was downregulated in patient MM cells compared with plasma cells from healthy donors. miR-26a overexpression inhibited proliferation, repressed migration, and induced apoptosis in MM cell lines. To identify the targets of miR-26a, RPMI8226-V-miR-26-GFP and RPMI8226-V-GFP cells were cultured using Stable isotope labeling by amino acids in cell culture (SILAC) medium followed by mass spectrometry analysis. CD38 protein was found downregulated in MM cells overexpressing miR-26a and subsequently confirmed to be a direct target of miR-26a by reporter assay and immunoblotting. In addition, when overexpressed, miR-26a had a synergistic effect with bortezomib (BTZ) or melphalan (MEL) treatment. To determine whether the inhibition of MM was due to inhibited CD38, we knocked down CD38 in MM cells and duplicated the MM inhibition observed with exogenous expression of miR-26a, whereas restoration of CD38 overcame the inhibition of miR-26a in MM cells. Furthermore, miR-26a inhibited CD38 expression provoked cell apoptosis and inhibited cell proliferation in human MM xenograft mouse models." @default.
• W4313374745 created "2023-01-06" @default.
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• W4313374745 date "2020-05-01" @default.
• W4313374745 modified "2023-10-12" @default.
• W4313374745 title "miR-26a as a novel potential therapeutic via inhibit CD38 translation and may overcome datatumumab resistance in multiple myeloma(MM)" @default.
• W4313374745 doi "https://doi.org/10.4049/jimmunol.204.supp.91.10" @default.
• W4313374745 hasPublicationYear "2020" @default.
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