Evidence map›Paper›PMID 31776466›Full record

ArticleLeukemia2020

CRL3-SPOP ubiquitin ligase complex suppresses the growth of diffuse large B-cell lymphoma by negatively regulating the MyD88/NF-κB signaling.

Xiaofeng Jin, Qing Shi, Qian Li, Linyi Zhou, Jian Wang, Lei Jiang, Xiaying Zhao, Kai Feng, Ting Lin, Zihan Lin and 21 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  4. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
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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

31 authors at 6 institutions in 2 countries.

Xiaofeng Jin *Department of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Qing Shi *State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China.
Qian LiDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Linyi ZhouDepartment of Science, National University of Singapore, Singapore, 117543, Singapore.
Jian WangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Lei JiangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Xiaying ZhaoState Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China.
Kai FengState Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China.
Ting LinDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Zihan LinDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Hui ZhuangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Jianye YangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Chongke HuDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Luyi ZhangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Liliang ShenDepartment of Urology, Department of Hematology, The Affiliated Yinzhou Renmin Hospital of Medical School of Ningbo University, Ningbo, 315040, China.
Ying LuDepartment of Urology, Department of Hematology, The Affiliated Yinzhou Renmin Hospital of Medical School of Ningbo University, Ningbo, 315040, China.
Jie ZhuDepartment of hepato-biliary-pancreatic Surgery, The Affiliated Ningbo Medical Center of LiHuiLi Hospital of Medical School of Ningbo University, Ningbo, 315048, China.
Haibiao WangDepartment of hepato-biliary-pancreatic Surgery, The Affiliated Ningbo Medical Center of LiHuiLi Hospital of Medical School of Ningbo University, Ningbo, 315048, China.
Honggang QiDepartment of Urology, The Affiliated Yinzhou Second Hospital of Medical School of Ningbo University, Ningbo, 315100, China.
Xiaodan MengDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Yang XiDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Jinchang PanDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Shuai FangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Haihua TianDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Chengwei ZhouDepartment of Thoracic Surgery, The Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Pingzhao ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Kun GaoClinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 200040, China.
Shi-Min ZhaoState Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China.
Yao LiState Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China.
Zhaohui GongDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo, 315211, China.
Chenji WangState Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, 200438, China. chenjiwang@fudan.edu.cn.
Ningbo University · CNState Key Laboratory of Genetic EngineeringFudan University · CNFudan University Shanghai Cancer Center · CNNational University of Singapore · SGShanghai First Maternity and Infant Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recurrent oncogenic mutations of MyD88 have been identified in a variety of lymphoid malignancies. Gain-of-function mutations of MyD88 constitutively activate downstream NF-κB signaling pathways, resulting in increased cellular proliferation and survival. However, whether MyD88 activity can be aberrantly regulated in MyD88-wild-type lymphoid malignancies remains poorly understood. SPOP is an adaptor protein of CUL3-based E3 ubiquitin ligase complex and frequently mutated genes in prostate and endometrial cancers. In this study, we reveal that SPOP binds to and induces the nondegradative ubiquitination of MyD88 by recognizing an atypical SPOP-binding motif in MyD88. This modification blocks Myddosome assembly and downstream NF-κB activation. SPOP is mutated in a subset of lymphoid malignancies, including diffuse large B-cell lymphoma (DLBCL). Lymphoid malignancies-associated SPOP mutants exhibited impaired binding to MyD88 and suppression of NF-κB activation. The DLBCL-associated, SPOP-binding defective mutants of MyD88 escaped from SPOP-mediated ubiquitination, and their effect on NF-κB activation is stronger than that of wild-type MyD88. Moreover, SPOP suppresses DLBCL cell growth in vitro and tumor xenograft in vivo by inhibiting the MyD88/NF-κB signaling. Therefore, SPOP acts as a tumor suppressor in DLBCL. Mutations in the SPOP-MyD88 binding interface may disrupt the SPOP-MyD88 regulatory axis and promote aberrant MyD88/NF-κB activation and cell growth in DLCBL.

Indexed as

ApoptosisCell ProliferationHumansLymphoma, Large B-Cell, DiffuseMutationMyeloid Differentiation Factor 88NF-kappa BNuclear ProteinsRepressor ProteinsTumor Cells, CulturedUbiquitinationUbiquitin-Protein LigasesUbiquitinsMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BNuclear ProteinsRepressor ProteinsSPOP protein, humanUbiquitin-Protein LigasesUbiquitins

Identifiers

PMID31776466
OpenAlexW2990337027

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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.