Scholarlink

<p>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. </p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

DEK facilitates bortezomib resistance of multiple myeloma by modulating ferroptosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月17日

查看全文
  • Huiquan Wang,
  • Jiafeng Zhang,
  • Lei Chen,
  • Hefei Ren,
  • Chang Liu,
  • Hong Kun Wu,
  • Huiying Qiu,
  • Juan Lu,
  • Lin Zhou

摘要

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.