Evidence map›Paper›PMID 36358786›Full record

ArticleCancers2022

The Histone Methyltransferase SETD8 Regulates the Expression of Tumor Suppressor Genes via H4K20 Methylation and the p53 Signaling Pathway in Endometrial Cancer Cells.

Asako Kukita, Kenbun Sone, Syuzo Kaneko, Eiryo Kawakami, Shinya Oki, Machiko Kojima, Miku Wada, Yusuke Toyohara, Yu Takahashi, Futaba Inoue and 14 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. SGSS05-NS3, a covalent SETD8 inhibitor that activates p53 pathway in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. C1QMolecular cancer · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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

24 authors at 6 institutions in 1 country.

Asako KukitaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Kenbun SoneDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-7218-6401
Syuzo KanekoDivision of Medical AI Research and Development, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0003-4558-9800
Eiryo KawakamiGraduate School of Medicine, Chiba University, Chiba 263-8522, Japan.
Shinya OkiNational Hospital Organization Tokyo Medical Center, Tokyo 152-8902, Japan.
Machiko KojimaTazuke Kofukai, Medical Research Institute, Kitano Hospital, Osaka 530-8480, Japan.
Miku WadaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Yusuke ToyoharaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Yu TakahashiDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Futaba InoueDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Saki TanimotoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Ayumi TaguchiDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-5491-3871
Tomohiko FukudaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0003-2711-3067
Yuichiro MiyamotoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Michihiro TanikawaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Mayuyo Mori-UchinoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0003-4545-0569
Tetsushi TsurugaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Takayuki IriyamaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Yoko MatsumotoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Kazunori NagasakaDepartment of Obstetrics and Gynecology, Teikyo University School of Medicine, Tokyo 173-0003, Japan.ORCID 0000-0002-0696-5175
Osamu Wada-HiraikeDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-3458-6711
Katsutoshi OdaDivision of Integrated Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-2468-9573
Ryuji HamamotoDivision of Medical AI Research and Development, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Yutaka OsugaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
The University of Tokyo · JPRIKEN Center for Advanced Intelligence Project · JPChiba University · JPKitano Hospital · JPTeikyo University · JPTokyo Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The histone methyltransferase SET domain-containing protein 8 (SETD8), which methylates histone H4 lysine 20 (H4K20) and non-histone proteins such as p53, plays key roles in human carcinogenesis. Our aim was to determine the involvement of SETD8 in endometrial cancer and its therapeutic potential and identify the downstream genes regulated by SETD8 via H4K20 methylation and the p53 signaling pathway. We examined the expression profile of SETD8 and evaluated whether SETD8 plays a critical role in the proliferation of endometrial cancer cells using small interfering RNAs (siRNAs). We identified the prognostically important genes regulated by SETD8 via H4K20 methylation and p53 signaling using chromatin immunoprecipitation sequencing, RNA sequencing, and machine learning. We confirmed that SETD8 expression was elevated in endometrial cancer tissues. Our in vitro results suggest that the suppression of SETD8 using siRNA or a selective inhibitor attenuated cell proliferation and promoted the apoptosis of endometrial cancer cells. In these cells, SETD8 regulates genes via H4K20 methylation and the p53 signaling pathway. We also identified the prognostically important genes related to apoptosis, such as those encoding KIAA1324 and TP73, in endometrial cancer.

Indexed as

chromatin immunoprecipitation sequencingendometrial cancerhistone methyltransferasesmachine learningSETD8 TP73

Identifiers

PMID36358786
PMCPMC9655767
OpenAlexW4308121382

What Socratic 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 Socratic graph.