Evidence map›Paper›PMID 25673502›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2015

Cadmium induces histone H3 lysine methylation by inhibiting histone demethylase activity.

Chunlian Xiao, Yin Liu, Chengfeng Xie, Wei Tu, Yujie Xia, Max Costa, Xue Zhou

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025
    Review
  5. Versatile JMJD proteins: juggling histones and much more.Trends in biochemical sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. [Luteolin has a significant protective effect against cadmium-induced injury in lung epithelial Beas-2B cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  17. Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021
    Review
  18. Review
  19. Review
  20. The Effects of Cadmium Toxicity.International journal of environmental research and public health · 2020
    Review
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

7 authors at 3 institutions in 2 countries.

Chunlian Xiao*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Yin Liu*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Chengfeng Xie*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Wei Tu*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Yujie Xia*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Max Costa*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York.
Xue Zhou*Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China and Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York xue.zhou@hust.edu.cn.
Huazhong University of Science and Technology · CNMinistry of Ecology and Environment · CNNew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium is an established human lung carcinogen with weak mutagenicity. However, the mechanisms underlying cadmium-induced carcinogenesis remain obscure. It has been suggested that epigenetic mechanisms may play a role in cadmium-induced carcinogenesis. In this study, we investigated the effects of cadmium on histone methylation and histone demethylases, and the role of histone methylation in transformation of immortalized normal human bronchial epithelial (BEAS-2B) cells. Exposure to 0.625, 1.25, 2.5, and 5.0 μM of cadmium for 6, 24, and 48 h increased global trimethylated histone H3 on lysine 4 (H3K4me3) and dimethylated histone H3 on lysine 9 (H3K9me2) in BEAS-2B cells compared with untreated cells, and most of these changes remained after the removal of cadmium (P < .05 or P < .01 for most modifications). Meanwhile, cadmium inhibited the activities of histone H3 on lysine 4 (H3K4) and histone H3 on lysine 9 (H3K9) demethylases which were detected by histone demethylation assay. However, there was no significant change in the protein levels of the H3K4 demethylase lysine-specific demethylase 5A (KDM5A) and the H3K9 demethylase lysine-specific demethylase 3A (KDM3A). Interestingly, during transformation of BEAS-2B cells by 20 weeks of exposure to 2.0 μM cadmium as assessed by anchorage-independent growth in soft agar, global H3K4me3, and H3K9me2 were significantly increased at 4 weeks (P < .05 or P < .01), whereas no significant change was observed at 8, 12, 16, and 20 weeks compared with control. Our study suggests that cadmium increases global H3K4me3 and H3K9me2 by inhibiting the activities of histone demethylases, and aberrant histone methylation that occurs early (48 h) and at 4 weeks is associated with cadmium-induced transformation of BEAS-2B cells at the early stage.

Indexed as

AnimalsCadmiumCattleCell LineEnzyme InhibitorsHistone DemethylasesHistonesLysineMethylationCadmiumEnzyme InhibitorsHistone DemethylasesHistonesLysinecadmiumcarcinogenesisepigeneticshistone demethylasehistone methylation

Identifiers

PMID25673502
PMCPMC4833035
OpenAlexW2165207473

What OpenQuestion holds

Textmetadata
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.