Evidence map›Paper›PMID 41249131›Full record

ArticleOncogenesis2025

YTHDF3 promotes breast cancer osteolytic bone metastasis by enhancing the translation of ZEB1 and SMAD5.

Lun Xu, Qian Yu, Xu Peihang, Kun Li, Bingnan Wang, Yang Shao, Mo Cheng, Wending Huang, Qianlan Yao, Xu Feng and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. WTAP Transcriptional Suppression by KLF9 Drives Osteoclastogenesis via MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. 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

13 authors.

Lun Xu *Department of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Qian Yu *Department of Cancer Center, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xu Peihang *Department of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Kun LiDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-5863-9865
Bingnan WangDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Yang ShaoGynecology Department of Traditional Chinese Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.ORCID http://orcid.org/0000-0002-3239-4265
Mo ChengDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Wending HuangDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Qianlan YaoDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xu FengDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Shaoli SongDepartment of Nuclear Medicine, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. shaoli-song@163.com.
Shuoer WangDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. wangshuoer@126.com.
Wangjun YanDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. yanwj@fudan.edu.cn.ORCID http://orcid.org/0000-0001-9178-0687

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone metastsis in advanced breast cancer patients are usually osteolytic. A better understanding of the mechanisms in osteolytic metastasis is critical for the development of new therapies. YTH domain-containing family protein 3 (YTHDF3) has been reported to function as an N6-methyladenosine (m6A)-modified mRNA regulator. In this study, we found YTDHF3 expression was associated with clinical characteristics of breast cancer patients. YTHDF3 expression influenced the migration and invasion capacity of breast cancer cells in vitro and in vivo, and low expression of YTHDF3 suppressed cancer cell-induced osteoclast differentiation and osteolytic bone destruction. Moreover, we found YTHDF3 enhanced the translation of zinc finger E-box-binding protein 1 (ZEB1) and SMAD family member 5 (SMAD5) by reading the m6A modification sites in their mRNAs and further promoted the epithelial-mesenchymal transition (EMT) of breast cancer cells. Enhanced expression of ZEB1 promoted the transcription of bone morphogenetic protein inhibitors such as NOG, FST and CCN2, which boosts osteolytic metastasis. Furthermore, we newly found Wnt family member 5B (WNT5B) expression was regulated by ZEB1, also involved in osteolytic process. In conclusion, YTHDF3 plays an important role in osteolytic metastasis and it may serve as a potential prognostic biomarker and therapeutic target for breast cancer bone metastasis.

Identifiers

PMID41249131
PMCPMC12623997

What Socratic holds

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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 Socratic graph.