Evidence map›Paper›PMID 41923628›Full record

ArticleCell reports. Medicine2026

A harmless-to-harmful switchable and spatiotemporally activated nano-CRISPR hierarchically amplifies ferroptosis in melanoma.

Chunqing Ou, Xianzhou Huang, Dongxue Huang, Rui Luo, Ruhan Chen, Xinchao Li, Xinyue Wu, Qinjie Wu, Changyang Gong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Chunqing OuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China; Department of Gastroenterology, Shanghai Institute of Pancreatic Diseases, Changhai Hospital, National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai 200433, China.
Xianzhou HuangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Dongxue HuangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Rui LuoDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Ruhan ChenDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Xinchao LiDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Xinyue WuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Qinjie WuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address: cellwqj@163.com.
Changyang GongDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address: chygong14@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis therapy faces challenges due to low lipid peroxide (LPO) levels. Herein, we develop a harmless-to-harmful switchable and spatiotemporally activated nano-CRISPR system (termed ARCHER) that sequentially amplifies ferroptosis sensitivity, iron ion levels, and reactive oxygen species (ROS) to amplify ferroptosis therapy efficiency. ARCHER targets cancer cells and releases CRISPR-Cas9 and Ce6Fe(III)Cl in response to hyaluronidase and tumor acidity. CRISPR-Cas9 sustains effective suppression of LPO-reducing protein GPX4. By persistently enhancing LPO accumulation through GPX4 downregulation, ARCHER primes cancer cells for ferroptosis and sensitizes them to subsequent interventions. Upon laser irradiation under acidic conditions, Ce6Fe(III)Cl undergoes spatiotemporal activation, transforming from inert form into cytotoxic Fe(III) ions and Ce6-generated ROS. Liberated Fe(III) and ROS synergistically amplify lipid peroxidation, driving LPO accumulation to trigger ferroptosis storm in sensitized cancer cells. In vivo studies demonstrated that ARCHER achieves 60% (3/5) tumor ablation with minimal off-target effects, validating its high therapeutic efficacy in ferroptosis-driven cancer treatment.

Indexed as

CRISPR-Cas SystemsFerroptosisMelanomaAnimalsCell Line, TumorHumansIronLipid PeroxidationLipid PeroxidesMicePhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesIronLipid PeroxidesPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen Speciescancer therapyCRISPR/Cas9ferroptosisharmless-harmful switchablespatiotemporally activated

Identifiers

PMID41923628
PMCPMC13130651

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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.