Evidence map›Paper›PMID 25875901›Full record

ArticlePloS one2015

3β-hydroxysterol δ24-reductase on the surface of hepatitis C virus-related hepatocellular carcinoma cells can be a target for molecular targeting therapy.

Makoto Saito, Takashi Takano, Tomohiro Nishimura, Michinori Kohara, Kyoko Tsukiyama-Kohara

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. 3Oncology research · 2025
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. HCV-Induced Oxidative Stress: Battlefield-Winning Strategy.Oxidative medicine and cellular longevity · 2016
    Review
  8. 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

5 authors at 2 institutions in 1 country.

Makoto SaitoDepartment of Experimental Phylaxiology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo Kumamoto-City, Kumamoto, Japan; Department of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.
Takashi TakanoDepartment of Experimental Phylaxiology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo Kumamoto-City, Kumamoto, Japan; Division of Veterinary Public Health, Nippon Veterinary and Life Science University, 1-7-1 Kyonan, Musashino, Tokyo, Japan.
Tomohiro NishimuraDepartment of Experimental Phylaxiology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo Kumamoto-City, Kumamoto, Japan; Chemo-Sero-Therapeutic Research Institute, Kikuchi Research Center, Kyokushi, Kikuchi, Kumamoto, Japan.
Michinori KoharaDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.
Kyoko Tsukiyama-KoharaDepartment of Experimental Phylaxiology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo Kumamoto-City, Kumamoto, Japan; Transboundary Animal Diseases Center, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, 1-21-24 Korimoto, Kagoshima, Japan; Laboratory of Animal Hygiene, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, 1-21-24 Korimoto, Kagoshima, Japan.
Kumamoto University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In our previous study, we demonstrated that 3β-hydroxysterol Δ24-reductase (DHCR24) was overexpressed in hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC), and that its expression was induced by HCV. Using a monoclonal antibody against DHCR24 (2-152a MAb), we found that DHCR24 was specifically expressed on the surface of HCC cell lines. Based on these findings, we aimed to establish a novel targeting strategy using 2-152a MAb to treat HCV-related HCC. In the present study, we examined the antitumor activity of 2-152a MAb. In the presence of complement, HCC-derived HuH-7 cells were killed by treatment with 2-152a MAb, which was mediated by complement-dependent cytotoxicity (CDC). In addition, the antigen recognition domain of 2-152a MAb was responsible for the unique anti-HCV activity. These findings demonstrate the feasibility of using 2-152a MAb for antibody therapy against HCV-related HCC. In addition, surface DHCR24 on HCC cells exhibited a functional property, agonist-induced internalization. We showed that 2-152a MAb-mediated binding of a cytotoxic agent (a saponin-conjugated secondary antibody) to surface DHCR24 led to significant cytotoxicity. This suggests that surface DHCR24 on HCC cells can function as a carrier for internalization. Therefore, surface DHCR24 could be a valuable target for HCV-related HCC therapy, and 2-152a MAb appears to be useful for this targeted therapy.

Indexed as

Antibodies, MonoclonalBlotting, WesternCarcinoma, HepatocellularCell ProliferationEnzyme-Linked Immunosorbent AssayFlow CytometryHepacivirusHepatitis C, ChronicHumansLiver NeoplasmsMolecular Targeted TherapyNerve Tissue ProteinsOxidoreductases Acting on CH-CH Group DonorsTumor Cells, CulturedVirus ReplicationAntibodies, MonoclonalDHCR24 protein, humanNerve Tissue ProteinsOxidoreductases Acting on CH-CH Group Donors

Identifiers

PMID25875901
PMCPMC4395381
OpenAlexW1981626694

What OpenQuestion holds

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LicenceCC BY
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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.