Evidence map›Paper›PMID 42831305›Full record

ArticleFEBS open bio2026

Selective elimination of quiescent cancer cells by dequalinium chloride via ROS-mediated ferroptosis.

Kotaro Miyamoto, Shiori Sakai, Minori Endo, Terigele, Mizuho Niibori, Taiki Morita, Yu Goto, Arisa Yoshida, Tomohiro Tanaka, Ning Lin and 5 more

Abstract read
In one paragraph

Article in FEBS open bio, 2026. 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

15 authors.

Kotaro MiyamotoSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Shiori SakaiSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Minori EndoSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
TerigeleSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Mizuho NiiboriSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Taiki MoritaInstitute of Integrated Research, Institute of Science Tokyo, Yokohama, Japan.
Yu GotoSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Arisa YoshidaSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Tomohiro TanakaSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Ning LinSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.
Takahiro KuchimaruCenter for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
Hiroyuki NakamuraInstitute of Integrated Research, Institute of Science Tokyo, Yokohama, Japan.ORCID https://orcid.org/0000-0002-4511-2984
Masahiro InoueGraduate School of Medicine, Kyoto University, Japan.
Shinae Kizaka-KondohSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.ORCID https://orcid.org/0000-0003-3085-5782
Tetsuya KadonosonoSchool of Life Science and Technology, Institute of Science Tokyo, Yokohama, Japan.ORCID https://orcid.org/0000-0001-6311-3203

Funding

Japan Society for the Promotion of Science 25K01589Ministry of Education, Culture, Sports, Science and Technology JPMXS0120330644Support for Pioneering Research Initiated by the Next Generation JPMJSP2180
6 · The paper itself

Abstract

Quiescent cancer cells (QCCs) drive tumor dormancy and recurrence through their resistance to conventional therapies. Furthermore, because QCCs rely on oxidative phosphorylation and maintain a fragile redox balance, we hypothesized that they harbor a targetable redox vulnerability. Here, we show that the mitochondria-targeted agent dequalinium chloride (DQ) selectively kills QCCs in hypoxia- and nutrient limitation-induced quiescent models, including H2228 cells, multicellular spheroids, and colorectal cancer organoids, while sparing proliferating cells and normal fibroblasts. DQ induces ROS accumulation beyond the survival threshold of QCCs, leading to lipid peroxidation and ferroptotic cell death, whereas proliferating cells undergo limited caspase-independent apoptosis. These findings highlight redox imbalance as an actionable vulnerability of QCCs and position DQ as a potential repurposed agent for eliminating QCCs.

Indexed as

dequalinium chlorideferroptosismitochondriaquiescent cancer cellsreactive oxygen species

Identifiers

PMID42831305
PMCPMC13635926

What OpenQuestion holds

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Registered trials

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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.