DEK facilitates bortezomib resistance of multiple myeloma by modulating ferroptosis

作者：Huiquan Wang, Jiafeng Zhang, Lei Chen, Hefei Ren, Chang Liu, Hong Wu, Huiying Qiu, Juan Lu, Lin Zhou · 发表于：Clinical and Experimental Medicine · 年份：2025 · DOI：10.1007/s10238-025-01673-4 · 被引用次数：2 · 研究领域：Multiple Myeloma Research and Treatments、Ubiquitin and proteasome pathways、Protein Degradation and Inhibitors

Multiple myeloma (MM) ranks as the second most prevalent blood cancer. In the treatment of MM, resistance to proteasome inhibitors like bortezomib (BTZ) is a significant issue, and the primary regulators and mechanisms are still not completely explored. As a result, this investigation aimed to uncover essential genes and mechanisms contributing to BTZ resistance in MM. Out of 359 differentially expressed genes, DEK oncogene (DEK) was pinpointed as the key drug-resistance gene in MM through bioinformatic analysis and was found to be overexpressed in MM patients. DEK was overexpressed in BTZ-resistant cell lines, enhancing the resistance of MM cells to bortezomib. Also, the depletion of DEK mitigated bortezomib resistance in MM cells by initiating ferroptosis. The findings indicated a novel role of DEK in the resistance of MM to bortezomib, which could inform new treatment strategies for BTZ-resistant MM.