Evidence map›Paper›PMID 40048740›Full record

ArticleBlood advances2025

Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma.

Jia Liu, Zilu Zhang, Wenbin Xu, Mingyuan Jia, Xinyi Zeng, Chengyu Wu, Ze Fu, Xiaoguang Xu, Chenjing Ye, Chao Wu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Jia LiuShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zilu ZhangShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenbin XuDepartment of General Practice, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mingyuan JiaShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xinyi ZengShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chengyu WuShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ze FuShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoguang XuShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chenjing YeDepartment of General Practice, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chao WuDepartment of General Practice, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hanzhang XuDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hu LeiDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-3288-5205
Yingli WuDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hua YanShanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-6067-4088

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractAberrant alternative splicing is one of the hallmarks of cancer and is potentially based on upregulated expression-of-splicing factors in some types of cancer. Our previous study suggested that the splicing factor RBM39 is significantly upregulated in multiple myeloma (MM) and that its upregulation is positively associated with poor prognosis. Here, we further demonstrate that the survival and proliferation of MM cells rely on RBM39 and that RBM39 knockdown inhibits the malignant growth of MM. Indisulam, a "molecular glue" that mediates the proteasomal degradation of RBM39, has potent suppressive effects on MM both in vitro and in vivo. Deletion of RBM39 results in extensively altered splicing, with mis-splicing of MEK5 verified to inhibit the malignant growth of MM. Full-length MEK5 plays a vital role in maintaining MM cell survival, whereas aberrant MEK5 isoforms with exon loss exhibit loss of function and a propensity for proteasomal degradation. Targeting RBM39 or MEK5 synergistically increases the cytotoxicity of bortezomib in MM cells via the inhibition of p65. Our study validates the specific mechanism of RBM39 in MM, providing an approach for broader targeting and optimized therapeutic strategies for MM.

Indexed as

Antineoplastic AgentsBortezomibMAP Kinase Kinase 5Multiple MyelomaRNA-Binding ProteinsAnimalsCell Line, TumorCell ProliferationDrug SynergismGene Expression Regulation, NeoplasticHumansMiceMitogen-Activated Protein Kinase 7Xenograft Model Antitumor AssaysAntineoplastic AgentsBortezomibMAPK7 protein, humanMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7RNA-Binding Proteins

Identifiers

PMID40048740
PMCPMC12034074

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.