Evidence map›Paper›PMID 28186963›Full record

ArticleOncotarget2017

An oral quinoline derivative, MPT0B392, causes leukemic cells mitotic arrest and overcomes drug resistant cancer cells.

Min-Wu Chao, Han-Li Huang, Wei-Chun HuangFu, Kai-Cheng Hsu, Yi-Min Liu, Yi-Wen Wu, Chao-Feng Lin, Yi-Lin Chen, Mei-Jung Lai, Hsueh-Yun Lee and 3 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Novel Methylselenoesters as Antiproliferative Agents.Molecules (Basel, Switzerland) · 2017
    Article
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

13 authors at 2 institutions in 1 country.

Min-Wu ChaoThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Han-Li HuangThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Wei-Chun HuangFuThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Kai-Cheng HsuThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Yi-Min LiuSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Yi-Wen WuSchool of Pharmacy, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
Chao-Feng LinThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Yi-Lin ChenThe Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Mei-Jung LaiTranslational Research Center, Taipei Medical University, Taipei 11031, Taiwan.
Hsueh-Yun LeeSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Jing-Ping LiouSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Che-Ming TengSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Chia-Ron YangSchool of Pharmacy, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
Taipei Medical University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite great advances in the treatment of acute leukemia, a renaissance of current chemotherapy needs to be improved. The present study elucidates the underlying mechanism of a new synthetic quinoline derivative, MPT0B392 (B392) against acute leukemia and its potential anticancer effect in drug resistant cells. B392 caused mitotic arrest and ultimately led to apoptosis. It was further demonstrated to be a novel microtubule-depolymerizing agent. The effects of oral administration of B392 showed relative potent anti-leukemia activity in an in vivo xenograft model. Further investigation revealed that B392 triggered induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of c-Jun N-terminal kinase (JNK). In addition, B392 enhanced the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells through inhibition of Akt/mTOR pathway and Mcl-1 protein expression, and also was active in the p-glycoprotein (p-gp)-overexpressing National Cancer Institute/Adriamycin-Resistant cells with little susceptibility to p-gp. Taken together, B392 has potential as an oral mitotic drug and adjunct treatment for drug resistant cancer cells.

Indexed as

Administration, OralAnimalsAntineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BCaspasesCell Line, TumorCell ProliferationDoxorubicinDrug Resistance, NeoplasmDrug SynergismHumansImmunohistochemistryJNK Mitogen-Activated Protein KinasesLeukemiaMembrane Potential, MitochondrialABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BCaspasesDoxorubicinJNK Mitogen-Activated Protein KinasesMCL1 protein, humanMTOR protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-aktQuinolinesSirolimusTOR Serine-Threonine KinasesTubulin Modulatorsacute leukemiadrug resistancemitotic arrestMPT0B392

Identifiers

PMID28186963
PMCPMC5438607
OpenAlexW2586156525

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.