Evidence map›Paper›PMID 39311951›Full record

ArticleJournal of cancer research and clinical oncology2024

Curcumin promotes ferroptosis in hepatocellular carcinoma via upregulation of ACSL4.

Yulang Jiang, Dengcheng Hui, Ziyang Pan, Yongxin Yu, Lu Liu, Xiaofan Yu, Chao Wu, Mingyu Sun

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In one paragraph

Article in Journal of cancer research and clinical oncology, 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
–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

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

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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

8 authors.

Yulang Jiang *Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Dengcheng Hui *Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Ziyang PanShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Yongxin YuShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Lu LiuShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Xiaofan YuShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Chao WuShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Mingyu SunShuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. mingyusun@shutcm.edu.cn.

Funding

Key Laboratory of Chronic Deficiency Liver Disease of the State Administration of Traditional Chinese Medicine of the People's Republic of China 20DZ2272200Major Project of Shanghai Municipal S and T Commission 19401972300Shandong Province Key R&D Program (Major Science and Technology Innovation Project 2021CXGC010509Shanghai Key Specialty of Traditional Chinese Clinical Medicine shslczdzk01201
6 · The paper itself

Abstract

backgroundFerroptosis, a novel iron-ion-dependent metabolic cell death mode with lipid peroxides as the main driving substrate, plays an irreplaceable role in the development and preventive treatment of hepatocellular carcinoma. Curcumin has potent pharmacological anti-tumor effects. AIM OF THE STUDY: We aimed to evaluate the ex vivo and in vivo cancer inhibitory activity of curcumin and its specific mechanism of action. MATERIALS AND

methodsWe used the hepatocellular carcinoma cell lines HepG2 and SMMC7721 to assess the direct inhibition of hepatocellular carcinoma proliferation by curcumin in vitro and a tumor xenograft model to evaluate the in vivo cancer inhibitory effect of curcumin.

resultsIn this study, we found that ferroptosis's inhibitors specifically reversed the curcumin-induced cell death pattern in HCC. After curcumin intervention, there was a substantial increase in MDA levels and iron ion levels, and a decrease in intracellular GSH levels. Meanwhile, the expression of GPX4 and SLC7A11 was significantly reduced at the protein levels, while ACSL4 and PTGS2 expression was significantly increased.

conclusionsThis study showed that curcumin significantly decreased the proliferation of HCC cells and significantly increased the sensitivity of ferroptosis. These results suggest that ACSL4 is a viable target for curcumin-induced ferroptosis in treating HCC.

Indexed as

Carcinoma, HepatocellularCell ProliferationCoenzyme A LigasesCurcuminFerroptosisLiver NeoplasmsUp-RegulationXenograft Model Antitumor AssaysAmino Acid Transport System y+AnimalsCell Line, TumorGene Expression Regulation, NeoplasticHep G2 CellsHumansMaleMiceAcsl4 protein, mouseAmino Acid Transport System y+Coenzyme A LigasesCurcuminPhospholipid Hydroperoxide Glutathione PeroxidaseSLC7A11 protein, humanACSL44Curcumin1Ferroptosis2Hepatocellular carcinoma 3Lipid peroxidation5

Identifiers

PMID39311951
PMCPMC11420324

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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.