Evidence map›Paper›PMID 33452347›Full record

ArticleScientific reports2021

Histamine H1 receptor antagonists selectively kill cisplatin-resistant human cancer cells.

Nobuki Matsumoto, Miku Ebihara, Shiori Oishi, Yuku Fujimoto, Tomoko Okada, Toru Imamura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Nobuki MatsumotoCell Regulation Laboratory, Bionics Program, Tokyo University of Technology Graduate School of Bionics, Computer and Media Science, Hachioji, Japan.
Miku EbiharaSchool of Bioscience and Biotechnology, Tokyo University of Technology, Hachioji, Tokyo, Japan.
Shiori OishiSchool of Bioscience and Biotechnology, Tokyo University of Technology, Hachioji, Tokyo, Japan.
Yuku FujimotoCell Regulation Laboratory, Bionics Program, Tokyo University of Technology Graduate School of Bionics, Computer and Media Science, Hachioji, Japan.
Tomoko OkadaNational Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki, Japan.
Toru ImamuraCell Regulation Laboratory, Bionics Program, Tokyo University of Technology Graduate School of Bionics, Computer and Media Science, Hachioji, Japan. imamurator@stf.teu.ac.jp.
Tokyo University of Technology · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer therapy is often hampered by the disease's development of resistance to anticancer drugs. We previously showed that the autonomously upregulated product of fibroblast growth factor 13 gene (FGF13; also known as FGF homologous factor 2 (FHF2)) is responsible for the cisplatin resistance of HeLa cisR cells and that it is likely responsible for the poor prognosis of cervical cancer patients treated with cisplatin. Here we show that cloperastine and two other histamine H1 receptor antagonists selectively kill HeLa cisR cells at concentrations that little affect parental HeLa S cells. The sensitivity of HeLa cisR cells to cloperastine was abolished by knocking down FGF13 expression. Cisplatin-resistant A549 cisR cells were similarly susceptible to cloperastine. H2, H3, and H4 receptor antagonists showed less or no cytotoxicity toward HeLa cisR or A549 cisR cells. These results indicate that histamine H1 receptor antagonists selectively kill cisplatin-resistant human cancer cells and suggest that this effect is exerted through a molecular mechanism involving autocrine histamine activity and high-level expression of FGF13. We think this represents a potential opportunity to utilize H1 receptor antagonists in combination with anticancer agents to treat cancers in which emergent drug-resistance is preventing effective treatment.

Indexed as

ApoptosisCell Line, TumorCisplatinDrug Resistance, NeoplasmFibroblast Growth FactorsGene ExpressionGene Expression Regulation, NeoplasticHeLa CellsHistamineHistamine H1 AntagonistsHistamine H2 AntagonistsHumansNeoplasmsPiperidinesReceptors, Histamine H1Cisplatincloperastinefibroblast growth factor 13Fibroblast Growth FactorsHistamineHistamine H1 AntagonistsHistamine H2 AntagonistsPiperidinesReceptors, Histamine H1

Identifiers

PMID33452347
PMCPMC7810706
OpenAlexW3124625304

What OpenQuestion holds

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LicenceCC BY
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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.