Evidence map›Paper›PMID 39930544›Full record

ArticleBreast cancer research : BCR2025

SMYD4 promotes MYH9 ubiquitination through lysine monomethylation modification to inhibit breast cancer progression.

Jin-Shuo Yang, Jun-Ming Cao, Rui Sun, Xue-Jie Zhou, Zhao-Hui Chen, Bo-Wen Liu, Xiao-Feng Liu, Yue Yu, Xin Wang

Abstract read
In one paragraph

Article in Breast cancer research : BCR, 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

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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. Identification of Epigenetic Regulator-Associated Genes in Keloid Disease Through Integrated Bulk and Single-Cell Transcriptomics With RT-qPCR Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Subtype-Specific mInternational journal of molecular sciences · 2026
    Article
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

9 authors.

Jin-Shuo Yang *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Jun-Ming Cao *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Rui Sun *The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Xue-Jie ZhouThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Zhao-Hui ChenThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Bo-Wen LiuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Xiao-Feng LiuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China.
Yue YuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China. yuyue@tmu.edu.cn.
Xin WangThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, China. wangxin@tjmuch.com.

Funding

National Natural Science Foundation of China 82172827National Natural Science Foundation of China 82172835National Natural Science Foundation of China 82473111
6 · The paper itself

Abstract

backgroundBreast cancer is the leading cause of female mortality worldwide. (SET And MYND Domain Containing 4) SMYD4 has been reported to be a tumour suppressor. However, the molecular mechanism of SMYD4 remains unclear.

methodsThe expression level of SMYD4 in breast cancer cells was detected by qRT-PCR and western blot. The effect of SMYD4 was verified in vitro and in vivo. The interaction between SMYD4 and MYH9 was investigated by co‑IP assay. The regulation of SMYD4 on WNT signaling pathway was detected by luciferase reporter assay and ChIP analysis.

resultsThis study found that SMYD4 downregulation was associated with poor prognosis. SMYD4 was performed as a tumor suppressor both in vitro and in vivo. SMYD4 was found to interact with the downstream protein MYH9 and impede WNT signaling pathway. Further studies revealed that SMYD4 impeded the binding of MYH9 to the CTNNB1 promoter region by promoting lysine monomethylation and ubiquitination degradation of MYH9.

conclusionsThese findings reveal the emerging character of SMYD4 in Wnt/β‑catenin signaling and bring new sights of gene interaction. The discovery of this SMYD4/MYH9/CTNNB1/WNT/β-Catenin signalling pathway axis suggests that SMYD4 is a potential therapeutic target for breast cancer.

Indexed as

Breast NeoplasmsHistone-Lysine N-MethyltransferaseLysineMyosin Heavy ChainsAnimalsbeta CateninCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMethylationMicePrognosisPromoter Regions, Geneticbeta CateninCTNNB1 protein, humanHistone-Lysine N-MethyltransferaseLysineMYH9 protein, humanMyosin Heavy ChainsBreast cancerMethylationMYH9SMYD4UbiquitinWnt/βcatenin signaling

Identifiers

PMID39930544
PMCPMC11812198

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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.