Evidence map›Paper›PMID 31114026›Full record

ArticleCell death and differentiation2020

Artemisinin compounds sensitize cancer cells to ferroptosis by regulating iron homeostasis.

Guo-Qing Chen, Fahad A Benthani, Jiao Wu, Deguang Liang, Zhao-Xiang Bian, Xuejun Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed, 2 pooled it
30.9field-weighted citation impact, top 1% 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

265 citing papers in PubMed, 2 syntheses or guidelines pooled it, 478 citations in OpenAlex.

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  4. Ferroptosis in cancer: molecular mechanisms, biological roles, and therapeutic significance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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205 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 3 countries.

Guo-Qing Chen *School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.
Fahad A Benthani *Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York City, NY, 10065, USA.
Jiao WuCell Biology Program, Memorial Sloan Kettering Cancer Center, New York City, NY, 10065, USA.
Deguang LiangCell Biology Program, Memorial Sloan Kettering Cancer Center, New York City, NY, 10065, USA.
Zhao-Xiang BianSchool of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China. bzxiang@hkbu.edu.hk.ORCID http://orcid.org/0000-0001-6206-1958
Xuejun JiangCell Biology Program, Memorial Sloan Kettering Cancer Center, New York City, NY, 10065, USA. jiangx@mskcc.org.
Memorial Sloan Kettering Cancer Center · USHong Kong Baptist University · HK

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Ferroptosis, Cellular Metabolism, and CancerR01CA204232 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JIANG, XUEJUN · 2017 to 2025
$4.1M
Role of the ULK1 Complex in AutophagyR01GM113013 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JIANG, XUEJUN · 2015 to 2018
$1.5M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA204232NIGMS NIH HHS R01 GM113013
6 · The paper itself

Abstract

The antimalarial drug artemisinin and its derivatives have been explored as potential anticancer agents, but their underlying mechanisms are controversial. In this study, we found that artemisinin compounds can sensitize cancer cells to ferroptosis, a new form of programmed cell death driven by iron-dependent lipid peroxidation. Mechanistically, dihydroartemisinin (DAT) can induce lysosomal degradation of ferritin in an autophagy-independent manner, increasing the cellular free iron level and causing cells to become more sensitive to ferroptosis. Further, by associating with cellular free iron and thus stimulating the binding of iron-regulatory proteins (IRPs) with mRNA molecules containing iron-responsive element (IRE) sequences, DAT impinges on IRP/IRE-controlled iron homeostasis to further increase cellular free iron. Importantly, in both in vitro and a mouse xenograft model in which ferroptosis was triggered in cancer cells by the inducible knockout of GPX4, we found that DAT can augment GPX4 inhibition-induced ferroptosis in a cohort of cancer cells that are otherwise highly resistant to ferroptosis. Collectively, artemisinin compounds can sensitize cells to ferroptosis by regulating cellular iron homeostasis. Our findings can be exploited clinically to enhance the effect of future ferroptosis-inducing cancer therapies.

Indexed as

AnimalsAntineoplastic AgentsArtemisininsAutophagyCell Line, TumorFemaleFerroptosisHomeostasisHumansIronIron-Regulatory ProteinsLysosomesMice, NudeNeoplasmsResponse ElementsAntineoplastic AgentsartemisininArtemisininsartenimolIronIron-Regulatory Proteins

Identifiers

PMID31114026
PMCPMC7205875
OpenAlexW2946704044

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.