Evidence map›Paper›PMID 36251033›Full record

ArticleCancer chemotherapy and pharmacology2022

Disulfiram enhances chemotherapeutic effects of doxorubicin liposomes against human hepatocellular carcinoma via activating ROS-induced cell stress response pathways.

Hai Lin, Fengjie Sun, Tingting Li, Yihan Zhang, Xiaochun Guo, Ming Li, Min Liang, Xinke Zhou, Zhiyuan Fang

Abstract read
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In one paragraph

Article in Cancer chemotherapy and pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Disulfiram in liver diseases: a double-edged sword.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  2. Article
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 at 3 institutions in 1 country.

Hai Lin *School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, China.
Fengjie Sun *The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510700, China.
Tingting LiReproductive Medicine Research Center, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
Yihan ZhangSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, China.
Xiaochun GuoSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, China.
Ming LiThe Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510700, China.
Min LiangThe Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510700, China.
Xinke ZhouThe Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510700, China.
Zhiyuan FangSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, China. fangjnu@126.com.ORCID 0000-0001-5622-8918
Guangdong University of Technology · CNGuangzhou Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIncreasing evidences have revealed the anti-cancer effect of disulfiram. Current disulfiram-based cancer therapies still have limitations, such as poor tumor-targeting ability and insufficient studies on anti-tumor mechanisms.

methodsIn the present study, tumor-targeting liposomes were prepared as drug carriers to increase retention of disulfiram in tumor cells. Then, anti-tumor efficacy of liposomes and the underlying mechanisms were investigated in in vitro, in vivo, and transcriptomic level.

resultsThe results showed that disulfiram enhanced sensitivity of human hepatocellular carcinoma cells to doxorubicin by 15-27-fold, and increased reactive oxygen species (ROS) production as well as caspase-dependent apoptosis. Inhibition of tumor migration and invasion by doxorubicin were further enhanced by disulfiram. In vivo study showed that disulfiram additive doxorubicin liposomes had better performance in suppressing tumor growth than single doxorubicin liposomes. Gene expression profiling found that cellular components destruction, cell stress, check point regulation, and immunoregulation were the main anti-tumor mechanisms of disulfiram. More importantly, disulfiram possessed a great potential to be a protein ubiquitination and murine double minute 4 (MDM4) targeting compound.

conclusionsDue to its low price and good safety, it is worth to repurposing disulfiram as a chemotherapeutic drug. Furthermore, MDM4 may act as a biomarker for observation the clinical effect of disulfiram-based treatment.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsCell Cycle ProteinsCell Line, TumorDisulfiramDoxorubicinHumansLiposomesMicePolyethylene GlycolsProto-Oncogene ProteinsReactive Oxygen SpeciesCell Cycle ProteinsDisulfiramDoxorubicinliposomal doxorubicinLiposomesMDM4 protein, humanPolyethylene GlycolsProto-Oncogene ProteinsReactive Oxygen SpeciesDisulfiramDoxorubicinHepatocellular carcinomaROSTumor targeting liposome

Identifiers

PMID36251033
OpenAlexW4306404687

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.