Evidence map›Paper›PMID 30031116›Full record

ArticleCancer letters2018

The positive inotropic agent DPI-201106 selectively reverses ABCB1-mediated multidrug resistance in cancer cell lines.

Sung-Han Hsiao, Megumi Murakami, Ni Yeh, Yan-Qing Li, Tai-Ho Hung, Yu-Shan Wu, Suresh V Ambudkar, Chung-Pu Wu

Abstract read
In one paragraph

Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 8 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

8 authors at 3 institutions in 2 countries.

Sung-Han HsiaoGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. Electronic address: johnson170_ya@hotmail.com.
Megumi MurakamiLaboratory of Cell Biology, CCR, NCI, NIH, Bethesda, United States. Electronic address: megumi.murakami@nih.gov.
Ni YehDepartment of Chemistry, Tunghai University, Taichung, Taiwan. Electronic address: qaz00120520@gmail.com.
Yan-Qing LiGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan; Department of Physiology and Pharmacology, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. Electronic address: hi9300190@yahoo.com.tw.
Tai-Ho HungDepartment of Chinese Medicine, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan; Department of Obstetrics and Gynecology, Taipei Chang Gung Memorial Hospital, Taipei, Taiwan. Electronic address: thh20@adm.cgmh.org.tw.
Yu-Shan WuDepartment of Chemistry, Tunghai University, Taichung, Taiwan. Electronic address: yushanwu@go.thu.edu.tw.
Suresh V AmbudkarLaboratory of Cell Biology, CCR, NCI, NIH, Bethesda, United States. Electronic address: ambudkar@mail.nih.gov.
Chung-Pu WuGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan; Department of Physiology and Pharmacology, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan; Department of Neurosurgery, Chang Gung Memorial Hospital, Linkou, Taiwan. Electronic address: wuchung@mail.cgu.edu.tw.
Chang Gung University · TWNational Institutes of Health · USTunghai University · TW

Funding

Biochemical Analysis of Multidrug Resistance-linked Transport ProteinsZIABC010030 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBUDKAR, SURESH · 2009 to 2025
$21.6M
Multidrug Resistance-linked Transport ProteinsZ01BC010030 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBUDKAR, SURESH · 1996 to 2008
$2.3M
Intramural NIH HHS Z01 BC010030
6 · The paper itself

Abstract

The overexpression of ABCB1 in cancer cells is a major factor contributing to the development of multidrug resistance (MDR) and treatment failure in cancer patients. Therefore, re-sensitization of MDR cancer cells to anticancer drugs remains an important aspect in chemotherapy. The progress in developing clinically applicable synthetic inhibitors of ABCB1 has been slow, mostly due to complications associated with intrinsic toxicities and unforeseen drug-drug interactions. Here, we explored the drug-repositioning approach for cancer therapy by targeting ABCB1-mediated MDR in human cancer cells. We found that DPI-201106, a positive inotropic agent, selectively inhibits the drug efflux function of ABCB1, and in doing so, re-sensitizes ABCB1-overexpressing MDR cancer cells to conventional anticancer drugs. Furthermore, the ATPase activity of ABCB1 and docking analysis of DPI-201106 in the drug-binding pocket of ABCB1 were determined to confirm the interaction between DPI-201106 and ABCB1 protein. In summary, we revealed an additional action and a potential clinical application of DPI-201106 to reverse ABCB1-mediated MDR in human cancer cells, which may be beneficial for cancer patients who have developed multidrug resistance and no longer respond to conventional chemotherapy, and should be further investigated.

Indexed as

AnimalsAntineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BCardiotonic AgentsCell Line, TumorCell SurvivalDrug RepositioningDrug Resistance, MultipleHEK293 CellsHumansMiceNeoplasmsNIH 3T3 CellsPiperazinesABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BCardiotonic AgentsDPI 201-106PiperazinesABCB1DPI-201106ModulatorMultidrug resistanceSodium channel

Identifiers

PMID30031116
PMCPMC6109596
OpenAlexW2883316115

What OpenQuestion holds

Textmetadata
LicenceTDM
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.