Evidence map›Paper›PMID 28055963›Full record

ArticleOncotarget2017

Emetine elicits apoptosis of intractable B-cell lymphoma cells with MYC rearrangement through inhibition of glycolytic metabolism.

Tomohiro Aoki, Kazuyuki Shimada, Akihiko Sakamoto, Keiki Sugimoto, Takanobu Morishita, Yuki Kojima, Satoko Shimada, Seiichi Kato, Chisako Iriyama, Shunsuke Kuno and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
2.2field-weighted citation impact, top 13% 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, 24 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

14 authors at 3 institutions in 1 country.

Tomohiro AokiDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kazuyuki ShimadaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akihiko SakamotoDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keiki SugimotoDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takanobu MorishitaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuki KojimaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Satoko ShimadaDepartment of Pathology and Clinical Laboratories, Nagoya University Hospital, Nagoya, Japan.
Seiichi KatoDepartment of Pathology and Clinical Laboratories, Nagoya University Hospital, Nagoya, Japan.
Chisako IriyamaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shunsuke KunoDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yasuhiko HaradaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akihiro TomitaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Fumihiko HayakawaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hitoshi KiyoiDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya University · JPNagoya University Hospital · JPFujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite improved clinical outcomes of diffuse large B-cell lymphoma, a certain proportion of patients still develop a primary refractory disease. To overcome these lymphomas that are intractable to existing treatment strategies, the tumor microenvironment has been identified as a potential therapeutic target. Here we describe our search for effective drugs for primary refractory lymphoma cells with MYC rearrangement. Through the drug screening of 3,440 known compounds, we identified a unique compound, emetine. This compound was effective against lymphoma cells with MYC rearrangement from two different patients that were co-cultured with cancer associated fibroblasts. Emetine induced the death of these cells with a half maximal inhibitory concentration of 312 nM and 506 nM, respectively. Subsequent analyses of the mechanism of action of emetine showed that the drug induced apoptosis of tumor cells via alteration of glucose metabolism through inhibition of hypoxia inducible factor-1α. Moreover, emetine inhibited the potential of cancer associated fibroblasts to support tumor cell viability in vitro and demonstrated significant inhibition of tumor growth in in vivo analyses. Emetine also induced cell death in other primary refractory lymphoma cells with MYC rearrangement. Our combined data indicate that emetine is a potential promising drug for the treatment of intractable lymphomas, which targets both the tumor and its microenvironment.

Indexed as

Xenograft Model Antitumor AssaysAnimalsApoptosisCancer-Associated FibroblastsCell SurvivalCoculture TechniquesEmetineGene RearrangementGlycolysisHumansImmunoblottingIn Situ Hybridization, FluorescenceLymphoma, Large B-Cell, DiffuseMice, Inbred NODMice, KnockoutMice, SCIDEmetineProtein Synthesis InhibitorsProto-Oncogene Proteins c-mycdiffuse large B-cell lymphomaemetineglycolysishigh-throughput drug screeningmicroenvironment

Identifiers

PMID28055963
PMCPMC5355079
OpenAlexW2563723550

What OpenQuestion holds

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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.