DUBR/miR-17-3p/TFRC/HO-1 Axis Promotes the Chemosensitivity of Multiple Myeloma.

Abstract

Long non-coding RNAs (lncRNAs) are intensively involved in the pathogenesis of multiple myeloma (MM). The purpose of this study was to investigate the potentials of DUBR in MM. Gene expression was determined using RT-qPCR and western blot. The release of ROS, MDA, ferrous iron, and GSH was detected with corresponding assays. Cell behavior was detected using CCK-8, colony formation, transwell, and PI staining assays. The binding sites between miR-17-3p and DUBR/TFRC was verified firmed by RIP, RNA pull-down, as well as luciferase assays. We found that low levels of DUBR predicted poor prognosis of MM patients. However, overexpressed DUBR enhanced the chemosensitivity of MM cells to bortezomib (BTZ), as well as promoted the ferroptosis of MM cells. DUBR sponged miR-17-3p to upregulate TFRC. However, TFRC knockdown abrogated the effects of overexpressed DUBR and promoted the aggressiveness of MM cells. In summary, DUBR promotes the chemosensitivity of MM cells to BTZ via regulating miR-17-3p/TFRC axis. Therefore, targeting DUBR may be a potential target for MM.