Evidence map›Paper›PMID 26769851›Full record

ArticleOncotarget2016

Inhibition of breast cancer cell motility with a non-cyclooxygenase inhibitory derivative of sulindac by suppressing TGFβ/miR-21 signaling.

Bin Yi, Hong Chang, Ruixia Ma, Xiangling Feng, Wei Li, Gary A Piazza, Yaguang Xi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 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 2 institutions in 2 countries.

Bin YiMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Hong ChangMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Ruixia MaMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Xiangling FengMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Wei LiDepartment of Pharmaceutical Science, University of Tennessee Health Science Center, Memphis, TN, USA.
Gary A PiazzaMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Yaguang XiMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
University of South Alabama · USUniversity of Tennessee Health Science Center · 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
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
MicroRNA and colorectal cancer chemopreventionR01CA192395 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI XI, YAGUANG · 2015 to 2019
$1.9M
MicroRNA, a new player for the NSAID sulindac to prevent colon cancer progressionR21CA182754 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI XI, YAGUANG · 2014 to 2015
$358k
MicroRNA, sulindac, and breast cancer chemopreventionR21CA160280 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A, XI, YAGUANG · 2012 to 2013
$346k
NCI NIH HHS 1R01CA131378NCI NIH HHS 1R01CA155638NCI NIH HHS 1R01CA192395NCI NIH HHS 1R21CA160280NCI NIH HHS 1R21CA182754NCI NIH HHS R01 CA131378NCI NIH HHS R01 CA155638NCI NIH HHS R01 CA192395NCI NIH HHS R21 CA160280NCI NIH HHS R21 CA182754
6 · The paper itself

Abstract

Compelling efficacy on intervention of tumorigenesis by nonsteroidal anti-inflammatory drugs (NSAIDs) has been documented intensively. However, the toxicities related to cyclooxygenase (COX) inhibition resulting in suppression of physiologically important prostaglandins limit their clinical use for human cancer chemoprevention. A novel derivative of the NSAID sulindac sulfide (SS), referred as sulindac sulfide amide (SSA), was recently developed, which lacks COX inhibitory activity, yet shows greater suppressive effect than SS on growth of various cancer cells. In this study, we focus on the inhibitory activity of SSA on breast tumor cell motility, which has not been studied previously. Our results show that SSA treatment at non-cytotoxic concentrations can specifically reduce breast tumor cell motility without influencing tumor cell growth, and the mechanism of action involves the suppression of TGFβ signaling by directly blocking Smad2/3 phosphorylation. Moreover, miR-21, a well-documented oncogenic miRNA for promoting tumor cell metastasis, was also found to be involved in inhibitory activity of SSA in breast tumor cell motility through the modulation of TGFβ pathway. In conclusion, we demonstrate that a non-COX inhibitory derivative of sulindac can inhibit breast tumor metastasis by a mechanism involving the TGFβ/miR-21 signaling axis.

Indexed as

ApoptosisBlotting, WesternBreast NeoplasmsCell MovementCell ProliferationChromatin ImmunoprecipitationFemaleFluorescent Antibody TechniqueHumansImmunoenzyme TechniquesMicroRNAsSulindacTransforming Growth Factor betaTumor Cells, CulturedWound HealingMicroRNAsMIRN21 microRNA, humanSulindacsulindac sulfide amideTransforming Growth Factor betabreast cancermetastasismicroRNAsulindacTGFβ

Identifiers

PMID26769851
PMCPMC4884969
OpenAlexW2280680201

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.