TRIM44通过促进ZEB1去泛素化促进多发性骨髓瘤的侵袭性。
TRIM44 facilitates aggressive behaviors in multiple myeloma through promoting ZEB1 deubiquitination.
作者信息
Qi Hui, Wang Jing, Cao Lixia
机构信息
Department of Hematology, Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Road, Huimin District, Hohhot, 010050, China.
Department of Rheumatology and Immunology, Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Road, Huimin District, Hohhot, 010050, China.
出版信息
Discov Oncol. 2025 Feb 27;16(1):248. doi: 10.1007/s12672-025-01933-5.
BACKGROUND
Tripartite motif-containing 44 (TRIM44) involves in various tumor development. This study investigated role of TRIM44 in multiple myeloma (MM).
MATERIALS AND METHODS
TRIM44 levels in bone marrow tissues and MM cell lines was detected by quantitative reverse transcription PCR (RT-qPCR). Cell viability, migration, and invasion of MM cells were evaluated under the interference of TRIM44 expression. The role of TRIM44 on regulating tumor growth in vivo was also investigated in subcutaneous tumor xenograft models. The protein interact between TRIM44 and Zinc Finger E-Box Binding Homeobox 1 (ZEB1) was also studied according IP followed by western blotting assay.
RESULTS
TRIM44 was all highly expressed in collected bone marrow tissues and MM cell lines. Cell viability, migration, and invasion of MM cells with low expression of TRIM44 was significantly inhibited. Over-expression of TRIM44 can down-regulate the ZEB1 ubiquitination to enhance the protein stability.
CONCLUSIONS
TRIM44 exerts as an oncogenic factor to induce the oncogenesis of MM by stabilizing ZEB1.
背景
含三联基序蛋白44（TRIM44）参与多种肿瘤的发展。本研究调查了TRIM44在多发性骨髓瘤（MM）中的作用。
材料与方法
通过定量逆转录PCR（RT-qPCR）检测骨髓组织和MM细胞系中TRIM44的水平。在TRIM44表达受到干扰的情况下，评估MM细胞的活力、迁移和侵袭能力。还在皮下肿瘤异种移植模型中研究了TRIM44在体内调节肿瘤生长的作用。通过免疫沉淀（IP）结合蛋白质印迹分析，研究了TRIM44与锌指E盒结合同源框1（ZEB1）之间的蛋白质相互作用。
结果
TRIM44在收集的骨髓组织和MM细胞系中均高表达。TRIM44低表达的MM细胞的活力、迁移和侵袭能力受到显著抑制。TRIM44的过表达可下调ZEB1的泛素化，以增强蛋白质稳定性。
结论
TRIM44作为一种致癌因子，通过稳定ZEB1诱导MM的发生。
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