Evidence map›Paper›PMID 29940898›Full record

ArticleBMC cancer2018

Dual effects of the Nrf2 inhibitor for inhibition of hepatitis C virus and hepatic cancer cells.

Yuko Murakami, Kazuo Sugiyama, Hirotoshi Ebinuma, Nobuhiro Nakamoto, Keisuke Ojiro, Po-Sung Chu, Nobuhito Taniki, Yoshimasa Saito, Toshiaki Teratani, Yuzo Koda and 7 more

Abstract read
In one paragraph

Article in BMC cancer, 2018. 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. Article
  2. Quassinoids as Promising Anti-cancer Agents.Current medicinal chemistry · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Brusatol: A potential anti-tumor quassinoid fromChinese herbal medicines · 2020
    Review
  9. Review
  10. Potential Applications of NRF2 Inhibitors in Cancer Therapy.Oxidative medicine and cellular longevity · 2019
    Review
  11. 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

17 authors.

Yuko MurakamiDivision of Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo, 105-8512, Japan.
Kazuo SugiyamaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan. sygiyamkz@a8.keio.jp.
Hirotoshi EbinumaDigestive Disease Center, International University of Health and Welfare, Mita Hospital, Tokyo, Japan.
Nobuhiro NakamotoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Keisuke OjiroDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Po-Sung ChuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Nobuhito TanikiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Yoshimasa SaitoDivision of Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo, 105-8512, Japan.
Toshiaki TerataniDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Yuzo KodaInnovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Takahiro SuzukiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Kyoko SaitoDepartment of Biochemistry and Cell Biology, National Institute of Infectious Disease, Tokyo, Japan.
Masayoshi FukasawaDepartment of Biochemistry and Cell Biology, National Institute of Infectious Disease, Tokyo, Japan.
Masanori IkedaDivision of Persistent and Oncogenic Viruses, Center for Chronic Viral Diseases, Kagoshima University Graduate School of Medicine, Tokyo, Japan.
Nobuyuki KatoDepartment of Molecular Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Takanori KanaiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University, Shinanomachi 35, Shinjuku-ku, Tokyo, 160-8582, Japan.
Hidetsugu SaitoDivision of Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Minato-ku, Tokyo, 105-8512, Japan. hsaito@a2.keio.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously showed that knockdown of nuclear factor E2-related factor 2 (Nrf2) resulted in suppression of hepatitis C virus (HCV) infection. In this study, whether brusatol, an Nrf2 inhibitor, has dual anti-HCV and anticancer effects was explored.

methodsThe anti-HCV effect of brusatol was investigated by analyzing HCV RNA and proteins in a hepatic cell line persistently-infected with HCV, HPI cells, and by analyzing HCV replication in a replicon-replicating hepatic cell line, OR6 cells. Then, dual anti-HCV and anticancer effects of brusatol and enhancement of the effects by the combination of brusatol with anticancer drugs including sorafenib, which has been reported to have the dual effects, were then investigated.

resultsBrusatol suppressed the persistent HCV infection at both the RNA and protein levels in association with a reduction in Nrf2 protein in the HPI cells. Analysis of the OR6 cells treated with brusatol indicated that brusatol inhibited HCV persistence by inhibiting HCV replication. Combination of brusatol with an anticancer drug not only enhanced the anticancer effect but also, in the case of the combination with sorafenib, strongly suppressed HCV infection.

conclusionsBrusatol has dual anti-HCV and anticancer effects and can enhance the comparable effects of sorafenib. There is therefore the potential for combination therapy of brusatol and sorafenib for HCV-related hepatocellular carcinoma.

Indexed as

Antineoplastic AgentsAntiviral AgentsCell Line, TumorHepatitis CHumansLiver NeoplasmsNF-E2-Related Factor 2QuassinsRNA, ViralSorafenibTranscriptomeVirus ReplicationAntineoplastic AgentsAntiviral AgentsbrusatolNFE2L2 protein, humanNF-E2-Related Factor 2QuassinsRNA, ViralSorafenibAnticancerAnti-HCVBrusatolChemotherapyHepatitis C virusHepatocellular carcinomaNuclear factor E2-related factor 2Sorafenib

Identifiers

PMID29940898
PMCPMC6019801

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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.