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• W2890545637 abstract "Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma, which is an aggressive malignancy with high variance of clinical features and response to the treatment. The proteasome inhibitor bortezomib (BTZ) has been demonstrated to suppress the progression of DLBCL, however, the underlying molecular mechanisms by which BTZ regulates the growth of DLBCL cells remain largely unknown. Increasing evidence has suggested that microRNAs (miRNAs) are novel targets of anti-cancer drugs to modulate the progression of cancers. Here, we showed BTZ treatment significantly inhibited the proliferation of DLBCL CRL-2630 cells. Mechanistically, exposure of BTZ up-regulated the expression of miR-198 in DLBCL cells. Depletion of miR-198 significantly reversed the inhibitory effect of BTZ on the proliferation of CRL-2630 cells. To further characterize the involvement of miR-198 in BTZ-induced growth defects of CRL-2630 cells, the downstream targets of miR-198 were predicted with the bioinformatics tools. The results showed that miR-198 bound the 3’-untranslated region (UTR) of the high mobility group AT-hook 1 (HMGA1) and suppressed the expression of HMGA1 in DLBCL cells. Consistently, BTZ treatment decreased the level of HMAG1 and inhibited the migration of DLBCL cells. Our results provided the possible mechanism by which BTZ suppressed the growth of DLBCL cells." @default.
• W2890545637 created "2018-09-27" @default.
• W2890545637 creator A5013367858 @default.
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• W2890545637 date "2018-12-01" @default.
• W2890545637 modified "2023-10-18" @default.
• W2890545637 title "Bortezomib inhibited the progression of diffuse large B-cell lymphoma via targeting miR-198" @default.
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• W2890545637 doi "https://doi.org/10.1016/j.biopha.2018.08.151" @default.
• W2890545637 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30216798" @default.
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