Evidence map›Paper›PMID 40790603›Full record

ArticleBreast cancer research : BCR2025

Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.

Kanako Hayashi, Takayuki Hoshii, Meng Ning, Makoto Matsumoto, Shintaro Izumi, Masaki Fukuyo, Bahityar Rahmutulla, Masahiko Tanabe, Atsushi Kaneda

Abstract read
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In one paragraph

Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Kanako HayashiDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Takayuki HoshiiDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan. hoshiit@chiba-u.jp.
Meng NingDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Makoto MatsumotoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Shintaro IzumiDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Masaki FukuyoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Bahityar RahmutullaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Masahiko TanabeDepartment of Breast and Endocrine Surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.

Funding

Japan Agency for Medical Research and Development JP24zf0127008Japan Agency for Medical Research and Development JP25ama221144Japan Society for the Promotion of Science JP22H04684Japan Society for the Promotion of Science JP22K19553
6 · The paper itself

Abstract

backgroundBreast cancer is the most common cancer in women worldwide. SETD1A, a histone H3 lysine-4 methyltransferase, is associated with poor prognosis in breast cancer. While both its enzymatic and non-enzymatic functions are implicated in cancer progression, the specific role of SETD1A in breast cancer remains unclear. This study aimed to elucidate the molecular mechanisms underlying SETD1A dependency in breast cancer.

methodsSETD1A-high breast cancer cell lines were identified using TCGA and DepMap databases, along with SETD1A knockdown experiments. A CRISPR knockout of SETD1A was performed in a doxycycline-inducible Cas9-expressing KPL-1 breast cancer cell line. RNA-seq, ChIP-seq, CRISPR-tiling screening, and rescue experiments with exogenous SETD1A mutants were performed to investigate the roles of SETD1A in breast cancer.

resultsSETD1A is highly expressed in estrogen receptor-positive / human epidermal growth factor receptor 2-negative (ER

conclusionsSETD1A promotes breast cancer cell replication through its non-enzymatic role via cyclin K, suggesting that the SETD1A-cyclin K axis could be a potential therapeutic target in breast cancer.

Indexed as

Breast NeoplasmsHistone-Lysine N-MethyltransferaseCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansPrognosisHistone-Lysine N-MethyltransferaseSetd1A protein, humanBreast cancerEpigenomeH3K4 methyltransferaseSETD1ATranscription

Identifiers

PMID40790603
PMCPMC12337470

What Socratic holds

Textmetadata
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 Socratic graph.