Evidence map›Paper›PMID 38299254›Full record

ArticleInternational journal of oncology2024

Inhibition of protein arginine methyltransferase 6 activates interferon signaling and induces the apoptosis of endometrial cancer cells via histone modification.

Futaba Inoue, Kenbun Sone, Kohei Kumegawa, Ryuta Hachijo, Eri Suzuki, Saki Tanimoto, Natsumi Tsuboyama, Kosuke Kato, Yusuke Toyohara, Yu Takahashi and 14 more

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

Article in International journal of oncology, 2024. 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
1.2field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. 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 3 institutions in 1 country.

Futaba InoueDepartment 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.
Kohei KumegawaCancer Cell Diversity Project, NEXT‑Ganken Program, Japanese Foundation for Cancer Research, Tokyo 135‑8550, Japan.
Ryuta HachijoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Eri SuzukiDepartment 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.
Natsumi TsuboyamaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Kosuke KatoDepartment 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.
Misako KusakabeDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Asako KukitaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Harunori HonjohDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Akira NishijimaDepartment 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.
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.
Takayuki IriyamaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Mayuyo MoriDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Osamu Wada-HiraikeDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Katsutoshi OdaDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
Hiromu SuzukiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Reo MaruyamaCancer Cell Diversity Project, NEXT‑Ganken Program, Japanese Foundation for Cancer Research, Tokyo 135‑8550, Japan.
Yutaka OsugaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113‑8655, Japan.
The University of Tokyo · JPJapanese Foundation For Cancer Research · JPSapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone modification, a major epigenetic mechanism regulating gene expression through chromatin remodeling, introduces dynamic changes in chromatin architecture. Protein arginine methyltransferase 6 (PRMT6) is overexpressed in various types of cancer, including prostate, lung and endometrial cancer (EC). Epigenome regulates the expression of endogenous retrovirus (ERV), which activates interferon signaling related to cancer. The antitumor effects of PRMT6 inhibition and the role of PRMT6 in EC were investigated, using epigenome multi‑omics analysis, including an assay for chromatin immunoprecipitation sequencing (ChIP‑seq) and RNA sequencing (RNA‑seq). The expression of PRMT6 in EC was analyzed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and immunohistochemistry (IHC). The prognostic impact of PRMT6 expression was evaluated using IHC. The effects of PRMT6‑knockdown (KD) were investigated using cell viability and apoptosis assays, as well as its effects on the epigenome, using ChIP‑seq of H3K27ac antibodies and RNA‑seq. Finally, the downstream targets identified by multi‑omics analysis were evaluated. PRMT6 was overexpressed in EC and associated with a poor prognosis. PRMT6‑KD induced histone hypomethylation, while suppressing cell growth and apoptosis. ChIP‑seq revealed that PRMT6 regulated genomic regions related to interferons and apoptosis through histone modifications. The RNA‑seq data demonstrated altered interferon‑related pathways and increased expression of tumor suppressor genes, including NK6 homeobox 1 and phosphoinositide‑3‑kinase regulatory subunit 1, following PRMT6‑KD. RT‑qPCR revealed that eight ERV genes which activated interferon signaling were upregulated by PRMT6‑KD. The data of the present study suggested that PRMT6 inhibition induced apoptosis through interferon signaling activated by ERV. PRMT6 regulated tumor suppressor genes and may be a novel therapeutic target, to the best of our knowledge, in EC.

Indexed as

Endometrial NeoplasmsHistonesApoptosisFemaleHistone CodeHumansInterferonsMaleNuclear ProteinsProtein-Arginine N-MethyltransferasesHistonesInterferonsNuclear ProteinsPRMT6 protein, humanProtein-Arginine N-Methyltransferasesapoptosishistone arginine methyltransferase; endometrial cancerinterferonPRMT6

Identifiers

PMID38299254
PMCPMC10836505
OpenAlexW4391360644

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.