Upregulation of miR-101-3p Overcomes Ibrutinib Resistance by Targeting ABCC5 in Diffuse Large B-Cell Lymphoma (DLBCL)

Diffuse large B-cell lymphoma (DLBCL) seriously threatens public health, and drug resistance is a formidable obstacle to DLBCL therapy. MicroRNAs (miRNAs) have been certified act as momentous regulator in of DLBCL. This study aimed ascertain the latent function mechanism miR-101-3p modulating cells ibrutinib. The differentially expressed miRNAs were identified by bioinformatics analysis GSE117063 GSE173080 datasets. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed measure expression levels ATP-binding cassette subfamily C member 5 (ABCC5). ibrutinib determined 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, Western blot assays. relationship between level ABCC5 analyzed using dual-luciferase reporter assay Pearson correlation test. MiR-101-3p significantly downregulated according results analysis. A low predicted Upregulation sensitized constructed ibrutinib-resistant (DLBCL/ibR). Our findings revealed that targeted miR-101-3p, abundantly DLBCL/ibR tissue samples cells. Furthermore, mimics overturned influences upregulation on played suppressive via inhibiting expression, which might represent potent therapeutic target for