Evidence map›Paper›PMID 38652216›Full record

ArticleJournal of cellular and molecular medicine2024

Dihydroartemisinin induces ferroptosis of hepatocellular carcinoma via inhibiting ATF4-xCT pathway.

Jie Ji, Ziqi Cheng, Jie Zhang, Jianye Wu, Xuanfu Xu, Chuanyong Guo, Jiao Feng

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

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
9.2field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Jie JiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Ziqi ChengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Jie ZhangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Jianye WuDepartment of Gastroenterology, Putuo People's Hospital, Tongji University, Shanghai, China.
Xuanfu XuDepartment of Gastroenterology, Shidong Hospital, University of Shanghai for Science and Technology, Shanghai, China.ORCID 0000-0002-4506-7220
Chuanyong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0002-6527-4673
Jiao FengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0001-5344-7242
Tongji University · CNUniversity of Shanghai for Science and Technology · CN

Funding

China Postdoctoral Science Foundation 2022M712412Shanghai Municipal Health Commission 20194Y0445The National Natural Science Foundation of China 82102956The Science and Technology Innovation Project of Shanghai Putuo District Health System ptkwws202303The Yangfan Project of Shanghai Science and Technology Commission 21YF1435400
6 · The paper itself

Abstract

Management of hepatocellular carcinoma (HCC) remains challenging due to population growth, frequent recurrence and drug resistance. Targeting of genes involved with the ferroptosis is a promising alternative treatment strategy for HCC. The present study aimed to investigate the effect of dihydroartemisinin (DHA) against HCC and explore the underlying mechanisms. The effects of DHA on induction of ferroptosis were investigated with the measurement of malondialdehyde concentrations, oxidised C11 BODIPY 581/591 staining, as well as subcutaneous xenograft experiments. Activated transcription factor 4 (ATF4) and solute carrier family 7 member 11 (SLC7A11 or xCT) were overexpressed with lentiviruses to verify the target of DHA. Here, we confirmed the anticancer effect of DHA in inducing ferroptosis is related to ATF4. High expression of ATF4 is related to worse clinicopathological prognosis of HCC. Mechanistically, DHA inhibited the expression of ATF4, thereby promoting lipid peroxidation and ferroptosis of HCC cells. Overexpression of ATF4 rescued DHA-induced ferroptosis. Moreover, ATF4 could directly bound to the SLC7A11 promoter and increase its transcription. In addition, DHA enhances the chemosensitivity of sorafenib on HCC in vivo and in vitro. These findings confirm that DHA induces ferroptosis of HCC via inhibiting ATF4-xCT pathway, thereby providing new drug options for the treatment of HCC.

Indexed as

Activating Transcription Factor 4Amino Acid Transport System y+ArtemisininsCarcinoma, HepatocellularFerroptosisLiver NeoplasmsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, NudeSignal TransductionActivating Transcription Factor 4Amino Acid Transport System y+ArtemisininsartenimolATF4 protein, humanSLC7A11 protein, humanSorafenibactivated transcription factor 4dihydroartemisininferroptosishepatocellular carcinomasolute carrier family 7 member 11sorafenib

Identifiers

PMID38652216
PMCPMC11037408
OpenAlexW4395034430

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.