Evidence map›Paper›PMID 36765890›Full record

ArticleCancers2023

Niclosamide Revitalizes Sorafenib through Insulin-like Growth Factor 1 Receptor (IGF-1R)/Stemness and Metabolic Changes in Hepatocellular Carcinoma.

Syue-Wei Peng, Mai-Huong T Ngo, Yung-Che Kuo, Ming-Hao Teng, Chin-Lin Guo, Hung-Cheng Lai, Te-Sheng Chang, Yen-Hua Huang

Abstract read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
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  6. Article
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  10. Review
  11. Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023
    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

8 authors.

Syue-Wei PengGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Mai-Huong T NgoDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Yung-Che KuoDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0002-9425-7389
Ming-Hao TengDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Chin-Lin GuoInstitute of Physics, Academia Sinica, Taipei 11529, Taiwan.
Hung-Cheng LaiDepartment of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, Taiwan.
Te-Sheng ChangSchool of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan 33382, Taiwan.ORCID 0000-0002-1581-6948
Yen-Hua HuangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0001-6020-9998

Funding

National Science and Technology Council 110-2314-B-038-034, 111-2314-B-038-089-MY3, 111-2314-B-182-047
6 · The paper itself

Abstract

Sorafenib is the first approved systemic targeting agent for advanced HCC; however, when used alone, drug resistance can result in considerably reduced efficacy. Here, we demonstrate that niclosamide, an antihelminthic agent approved by the US Food and Drug Administration, can be repurposed to increase sorafenib sensitivity in sorafenib-resistant HCC cells. We generated sorafenib-resistant HCC cell lines (HepG2215_R and Hep3B_R) with elevated IGF-1R levels and strong properties in terms of stemness and epithelial-mesenchymal transition. Niclosamide was found to increase sorafenib sensitivity effectively in both cell lines and their organoids. The underlying mechanism involves the modulation of cancer stemness, IGF-1R/p-IGF1R/OCT4, and metabolic changes. The combination of sorafenib and niclosamide, but not linsitinib, effectively suppressed the IGF-1R/OCT4 expressions, yielded a synergistic combination index (CI), and attenuated stemness-related properties such as secondary tumor sphere formation and cell migration in sorafenib-resistant HCC cells. Notably, niclosamide significantly suppressed the sorafenib-induced IGF-1R phosphorylation prompted by IGF-1 treatment. Niclosamide effectively downregulated the sorafenib-induced gene expression associated with glycolysis (

Indexed as

HCC sorafenib resensitizationIGF-1Rmetabolic changeniclosamideorganoid

Identifiers

PMID36765890
PMCPMC9913083

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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.