Evidence map›Paper›PMID 34214254›Full record

ArticleMolecular oncology2021

EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression.

Jinkwon Lee, Kwangho Kim, Tae Young Ryu, Cho-Rok Jung, Moo-Seung Lee, Jung Hwa Lim, Kunhyang Park, Dae-Soo Kim, Mi-Young Son, Ryuji Hamamoto and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. The Functional Role and Regulatory Mechanism of FTO mInternational journal of molecular sciences · 2023
    Article
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 3 countries.

Jinkwon LeeKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Kwangho KimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Tae Young RyuKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Cho-Rok JungKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Moo-Seung LeeKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Jung Hwa LimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Kunhyang ParkKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Dae-Soo KimKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Mi-Young SonKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Ryuji HamamotoDivision of Molecular Modification and Cancer Biology, National Cancer Center, Tokyo, Japan.
Hyun-Soo ChoKorea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.ORCID 0000-0002-8242-9390
Korea Research Institute of Bioscience and Biotechnology · KRNational Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dozens of histone methyltransferases have been identified and biochemically characterized, but the pathological roles of their dysfunction in human diseases such as cancer remain largely unclear. Here, we demonstrate the involvement of EHMT1, a histone lysine methyltransferase, in lung cancer. Immunohistochemical analysis indicated that the expression levels of EHMT1 are significantly elevated in human lung carcinomas compared with non-neoplastic lung tissues. Through gene ontology analysis of RNA-seq results, we showed that EHMT1 is clearly associated with apoptosis and the cell cycle process. Moreover, FACS analysis and cell growth assays showed that knockdown of EHMT1 induced apoptosis and G1 cell cycle arrest via upregulation of CDKN1A in A549 and H1299 cell lines. Finally, in 3D spheroid culture, compared to control cells, EHMT1 knockdown cells exhibited reduced aggregation of 3D spheroids and clear upregulation of CDKN1A and downregulation of E-cadherin. Therefore, the results of the present study suggest that EHMT1 plays a critical role in the regulation of cancer cell apoptosis and the cell cycle by modulating CDKN1A expression. Further functional analyses of EHMT1 in the context of human tumorigenesis may aid in the development of novel therapeutic strategies for cancer.

Indexed as

Lung NeoplasmsApoptosisCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHumansLungCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21EHMT1 protein, humanHistone-Lysine N-MethyltransferaseapoptosisCDKN1Acell cycleEHMT1lung cancer

Identifiers

PMID34214254
PMCPMC8564652
OpenAlexW3174511218

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.