Evidence map›Paper›PMID 24626598›Full record

ArticleInternational journal of oncology2014

Masitinib antagonizes ATP-binding cassette subfamily G member 2-mediated multidrug resistance.

Rishil J Kathawala, Jun-Jiang Chen, Yun-Kai Zhang, Yi-Jun Wang, Atish Patel, De-Shen Wang, Tanaji T Talele, Charles R Ashby, Zhe-Sheng Chen

Abstract read
In one paragraph

Article in International journal of oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Masitinib analogues with theJournal of King Saud University. Science · 2023
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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

9 authors.

Rishil J KathawalaDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Jun-Jiang ChenDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Yun-Kai ZhangDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Yi-Jun WangDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Atish PatelDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
De-Shen WangDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Tanaji T TaleleDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Charles R AshbyDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.

Funding

Targeting MRP7 to Overcome Drug Resistance for Ovarian Cancer Therapy by TaxanesR15CA143701 · NCI · ST. JOHN'S UNIVERSITY · PI CHEN, ZHE-SHENG · 2010 to 2010
$245k
NCI NIH HHS 1R15CA143701NCI NIH HHS R15 CA143701
6 · The paper itself

Abstract

In this in vitro study, we determined whether masitinib could reverse multidrug resistance (MDR) in cells overexpressing the ATP binding cassette subfamily G member 2 (ABCG2) transporter. Masitinib (1.25 and 2.5 µM) significantly decreases the resistance to mitoxantrone (MX), SN38 and doxorubicin in HEK293 and H460 cells overexpressing the ABCG2 transporter. In addition, masitinib (2.5 µM) significantly increased the intracellular accumulation of [(3)H]-MX, a substrate for ABCG2, by inhibiting the function of ABCG2 and significantly decreased the efflux of [(3)H]-MX. However, masitinib (2.5 µM) did not significantly alter the expression of the ABCG2 protein. In addition, a docking model suggested that masitinib binds within the transmembrane region of a homology-modeled human ABCG2 transporter. Overall, our in vitro findings suggest that masitinib reverses MDR to various anti-neoplastic drugs in HEK293 and H460 cells overexpressing ABCG2 by inhibiting their transport activity as opposed to altering their levels of expression.

Indexed as

Antineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2BenzamidesCell Line, TumorDrug Resistance, MultipleDrug SynergismHEK293 CellsHumansMitoxantroneModels, MolecularMolecular Docking SimulationNeoplasm ProteinsPiperidinesProtein Kinase InhibitorsPyridinesABCG2 protein, humanAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2BenzamidesmasitinibMitoxantroneNeoplasm ProteinsPiperidinesProtein Kinase InhibitorsPyridinesThiazoles

Identifiers

PMID24626598
PMCPMC4027943

What OpenQuestion holds

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Read underepoch 390

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.