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<p>Malignant plasma cell proliferation characterizes multiple myeloma (MM), a hematologic disease. Bortezomib (BTZ) is a protease inhibitor that has been approved for the treatment of MM. Nevertheless, the effectiveness of BTZ is frequently impeded by drug resistance, and the mechanisms responsible for this phenomenon remain incompletely understood. A growing body of evidence indicates that N6-methyladenosine (m6A) plays crucial roles in a wide range of biological functions. However, the impact of m6A on the response of MM cells to BTZ is poorly understood. In our recent research, we discovered that METTL3 facilitated the m6A alteration of lncRNA H19, providing MM cells with resistance to BTZ. Additional examination revealed that H19 functioned as a sponge to negatively regulate the expression of miR-184 in MM cells. Furthermore, we discovered that H19 binds to miR-184, a tumor suppressor, in MM cells. In MM cells, miR184 can suppress the expression of CARM1 by targeting its 3′-UTR. In conclusion, rescue trials have validated the significance of the METTL3/H19/miR-184/CARM1 pathway in determining the susceptibility of cells to BTZ. Consequently, directing efforts toward this pathway could prove to be a powerful approach for enhancing the effectiveness of BTZ for MM therapy.</p>

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N6-methyladenosine-mediated upregulation of H19 promotes resistance to bortezomib by modulating the miR-184/CARM1 axis in multiple myeloma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月1日

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  • Gang Wang,
  • Wenping Wu,
  • Donghua He,
  • Jiaheng Wang,
  • Hongwei Kong,
  • Wenjun Wu

摘要

Malignant plasma cell proliferation characterizes multiple myeloma (MM), a hematologic disease. Bortezomib (BTZ) is a protease inhibitor that has been approved for the treatment of MM. Nevertheless, the effectiveness of BTZ is frequently impeded by drug resistance, and the mechanisms responsible for this phenomenon remain incompletely understood. A growing body of evidence indicates that N6-methyladenosine (m6A) plays crucial roles in a wide range of biological functions. However, the impact of m6A on the response of MM cells to BTZ is poorly understood. In our recent research, we discovered that METTL3 facilitated the m6A alteration of lncRNA H19, providing MM cells with resistance to BTZ. Additional examination revealed that H19 functioned as a sponge to negatively regulate the expression of miR-184 in MM cells. Furthermore, we discovered that H19 binds to miR-184, a tumor suppressor, in MM cells. In MM cells, miR184 can suppress the expression of CARM1 by targeting its 3′-UTR. In conclusion, rescue trials have validated the significance of the METTL3/H19/miR-184/CARM1 pathway in determining the susceptibility of cells to BTZ. Consequently, directing efforts toward this pathway could prove to be a powerful approach for enhancing the effectiveness of BTZ for MM therapy.