Evidence map›Paper›PMID 28276667›Full record

ArticleJournal of biomedical research2016

Sulindac sulfide selectively increases sensitivity of ABCC1 expressing tumor cells to doxorubicin and glutathione depletion.

Jason D Whitt, Adam B Keeton, Bernard D Gary, Larry A Sklar, Kamlesh Sodani, Zhe-Sheng Chen, Gary A Piazza

Abstract read
In one paragraph

Article in Journal of biomedical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 18 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

7 authors at 5 institutions in 1 country.

Jason D WhittDepartment of Biochemistry, University of Mississippi Medical Center Cancer Institute, Jackson, MS 39216, USA.
Adam B KeetonDrug Discovery Research Center, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.
Bernard D GaryDrug Discovery Research Center, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.
Larry A SklarDepartment of Pathology, The University of New Mexico, Albuquerque, NM 87131, USA.
Kamlesh SodaniDepartment of Pharmaceutical Sciences, St. John's University, New York, NY 11439, USA.
Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, St. John's University, New York, NY 11439, USA.
Gary A PiazzaDrug Discovery Research Center, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.
Columbia Southern University · USSt. John's University · USUniversity of Mississippi Medical Center · USUniversity of New Mexico · USUSA Mitchell Cancer Institute · US

Funding

Selective anti-cancer activity of sulindac derivatives on KRAS mutant colon tumor cells by inducing ROSR01CA131378 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2008 to 2019
$5.2M
Development of a novel sulindac amide for colorectal cancer chemopreventionR01CA148817 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2010 to 2015
$2.4M
Phosphodiesterase 5: A Novel Target and Inhibitor for Breast Cancer ChemopreventionR01CA155638 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2012 to 2017
$2.3M
Phosphodiesterase 10A, a novel target for lung cancer chemopreventionR01CA197147 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2016 to 2020
$1.9M
NCI NIH HHS R01 CA131378NCI NIH HHS R01 CA148817NCI NIH HHS R01 CA155638NCI NIH HHS R01 CA197147
6 · The paper itself

Abstract

ATP-binding cassette (ABC) transporters ABCC1 (MRP1), ABCB1 (P-gp), and ABCG2 (BCRP) contribute to chemotherapy failure. The primary goals of this study were to characterize the efficacy and mechanism of the nonsteroidal anti-inflammatory drug (NSAID), sulindac sulfide, to reverse ABCC1 mediated resistance to chemotherapeutic drugs and to determine if sulindac sulfide can influence sensitivity to chemotherapeutic drugs independently of drug efflux. Cytotoxicity assays were performed to measure resistance of ABC-expressing cell lines to doxorubicin and other chemotherapeutic drugs. NSAIDs were tested for the ability to restore sensitivity to resistance selected tumor cell lines, as well as a large panel of standard tumor cell lines. Other experiments characterized the mechanism by which sulindac sulfide inhibits ABCC1 substrate and co-substrate (GSH) transport in isolated membrane vesicles and intact cells. Selective reversal of multi-drug resistance (MDR), decreased efflux of doxorubicin, and fluorescent substrates were demonstrated by sulindac sulfide and a related NSAID, indomethacin, in resistance selected and engineered cell lines expressing ABCC1, but not ABCB1 or ABCG2. Sulindac sulfide also inhibited transport of leukotriene C

Indexed as

doxorubicinglutathioneMRP1multi-drug resistancesulindac

Identifiers

PMID28276667
PMCPMC4820889
OpenAlexW2470044349

What OpenQuestion holds

Textmetadata
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.