Evidence map›Paper›PMID 37121971›Full record

ArticleExperimental & molecular medicine2023

Epigenetic regulation of SMAD3 by histone methyltransferase SMYD2 promotes lung cancer metastasis.

Kwangho Kim, Tae Young Ryu, Eunsun Jung, Tae-Su Han, Jinkwon Lee, Seon-Kyu Kim, Yu Na Roh, Moo-Seung Lee, Cho-Rok Jung, Jung Hwa Lim and 6 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
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  3. Article
  4. Review
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  6. Review
  7. LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  8. Review
  9. Apoptosis-Inducing Effects ofJournal of microbiology and biotechnology · 2025
    Article
  10. Therapeutic Potential ofJournal of microbiology and biotechnology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
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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

16 authors.

Kwangho Kim *Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Tae Young Ryu *Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Eunsun Jung *Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Tae-Su Han *Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Jinkwon LeeKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Seon-Kyu KimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0002-4176-5187
Yu Na RohKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Moo-Seung LeeKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Cho-Rok JungKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Jung Hwa LimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Ryuji HamamotoDivision of Molecular Modification and Cancer Biology, National Cancer Center, Tokyo, Japan.
Hye Won LeeDepartment of Pathology, Keimyung University School of Medicine, Daegu, Republic of Korea.
Keun HurDepartment of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea. KeunHur@knu.ac.kr.ORCID http://orcid.org/0000-0002-6944-2718
Mi-Young SonKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea. myson@kribb.re.kr.ORCID http://orcid.org/0000-0001-7590-8812
Dae-Soo KimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea. kds2465@kribb.re.kr.ORCID http://orcid.org/0000-0002-4999-1613
Hyun-Soo ChoKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea. chohs@kribb.re.kr.ORCID http://orcid.org/0000-0002-8242-9390

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic alterations, especially histone methylation, are key factors in cell migration and invasion in cancer metastasis. However, in lung cancer metastasis, the mechanism by which histone methylation regulates metastasis has not been fully elucidated. Here, we found that the histone methyltransferase SMYD2 is overexpressed in lung cancer and that knockdown of SMYD2 could reduce the rates of cell migration and invasion in lung cancer cell lines via direct downregulation of SMAD3 via SMYD2-mediated epigenetic regulation. Furthermore, using an in vitro epithelial-mesenchymal transition (EMT) system with a Transwell system, we generated highly invasive H1299 (In-H1299) cell lines and observed the suppression of metastatic features by SMYD2 knockdown. Finally, two types of in vivo studies revealed that the formation of metastatic tumors by shSMYD2 was significantly suppressed. Thus, we suggest that SMYD2 is a potential metastasis regulator and that the development of SMYD2-specific inhibitors may help to increase the efficacy of lung cancer treatment.

Indexed as

HistonesLung NeoplasmsCell Line, TumorCell ProliferationEpigenesis, GeneticEpithelial-Mesenchymal TransitionHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHumansSmad3 ProteinHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesSmad3 ProteinSMAD3 protein, humanSMYD2 protein, human

Identifiers

PMID37121971
PMCPMC10238379

What OpenQuestion 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 OpenQuestion graph.