Evidence map›Paper›PMID 39885217›Full record

ArticleNature communications2025

EZH2 serves as a viable therapeutic target for myeloma-induced osteolytic bone destruction.

Rui Liu, Zongwei Li, Rui Chen, Zhihong Fang, Zhiqiang Liu, Huan Liu

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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

6 authors.

Rui Liu *Cancer Research Center, School of Medicine, Xiamen University, Xiamen, China.
Zongwei Li *School of Life Sciences, Anhui Medical University, Hefei, Anhui, China.
Rui ChenCancer Research Center, School of Medicine, Xiamen University, Xiamen, China.
Zhihong FangDepartment of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, School of Medicine, Xiamen University, Xiamen, China.
Zhiqiang LiuShandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China. zqliu@sdfmu.edu.cn.ORCID http://orcid.org/0000-0002-0677-8097
Huan LiuCancer Research Center, School of Medicine, Xiamen University, Xiamen, China. huanliu@xmu.edu.cn.ORCID http://orcid.org/0000-0002-2314-5136

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82170197Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation) 2022D015Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation) 2024R1036Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2024A1515010076Shenzhen Science and Technology Innovation Commission JCYJ20220530143403007
6 · The paper itself

Abstract

Myelomatous bone disease is a complication characterized by lytic bone lesions, reduced bone formation, bone pain, and increased fracture risk. Understanding these underlying mechanisms is crucial for developing effective therapeutic approaches. Here we show the role of enhancer of zeste homolog 2 (EZH2) in bone lesions induced by myeloma cells. Our research reveals that cytokines produced by myeloma-associated adipocytes activate the expression of EZH2 in myeloma cells. Furthermore, we find that EZH2 forms a transcriptional repression complex with transcription factor AP2α. This complex promotes trimethylation at lysine 27 of histone H3 (H3K27me3) in the promoter region of the tumor suppressor gene EMP1, resulting in transcriptional silencing. EMP1 silencing leads to increased myeloma cell proliferation and the concomitant secretion of osteolytic cytokines that contribute to bone destruction. Importantly, EZH2 inhibitors effectively treat myeloma-induced osteolytic lesions. Thus, targeting EZH2 represents a potential therapeutic strategy for preventing and managing myeloma bone disease.

Indexed as

Enhancer of Zeste Homolog 2 ProteinMultiple MyelomaOsteolysisAnimalsCell Line, TumorCell ProliferationCytokinesGene Expression Regulation, NeoplasticHistonesHumansMethylationMiceCytokinesEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistones

Identifiers

PMID39885217
PMCPMC11782520

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.