Evidence map›Paper›PMID 26376791›Full record

ArticleMolecular cancer2015

Activation of peroxisome proliferator-activated receptor gamma is crucial for antitumoral effects of 6-iodolactone.

Mario Nava-Villalba, Rosa E Nuñez-Anita, Alexander Bontempo, Carmen Aceves

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03688958 (Effect of Dietary Iodine Supplementation on the Proliferation of Breast Cancer), which is not on this map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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.

NCT03688958 phase2unknown statusnot on this map

Effect of Dietary Iodine Supplementation on the Proliferation of Breast Cancer

TypeinterventionalSponsorUniversidad Nacional Autonoma de MexicoRan2005 to 2020Enrolled120ConditionsBreast CancerArmsPlacebo, iodine, FEC/TE Placebo, FEC/TE iodine
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 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

4 authors at 2 institutions in 1 country.

Mario Nava-VillalbaInstituto de Neurobiología, Universidad Nacional Autónoma de México-Juriquilla, Boulevard Juriquilla 3001, Juriquilla, Querétaro, CP 76230, Mexico. marionava23@unam.mx.
Rosa E Nuñez-AnitaFacultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, Mexico. re.nunez.anita@gmail.com.
Alexander BontempoInstituto de Neurobiología, Universidad Nacional Autónoma de México-Juriquilla, Boulevard Juriquilla 3001, Juriquilla, Querétaro, CP 76230, Mexico. bontix77@yahoo.it.
Carmen AcevesInstituto de Neurobiología, Universidad Nacional Autónoma de México-Juriquilla, Boulevard Juriquilla 3001, Juriquilla, Querétaro, CP 76230, Mexico. caracev@unam.mx.
Universidad Nacional Autónoma de México · MXUniversidad Michoacana de San Nicolás de Hidalgo · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMolecular iodine (I2) exhibits antiproliferative and apoptotic effects on in vivo and in vitro cancer models. These effects are thought to be mediated by an iodinated arachidonic acid derivative, 6-iodolactone (6IL), and one of the proposed mechanisms is that 6IL activates Peroxisome Proliferator-Activated Receptors type gamma (PPARG). These receptors have been implicated in the inhibition of carcinogenic processes, in addition to their classical role in maintaining lipid and glucose homeostasis. The aim of this study was to determine whether PPARG participates in the 6IL antiproliferative and apoptotic effects on the mammary cancer cell line MCF-7.

methodsThe 6IL/PPARG complex was inhibited by the PPARG antagonist GW9662, in both an endogenous and overexpressed (adenoviral vector infection) context, and stable PPARG-knockdown MCF-7 cells (RNA interference, confirmed with hydrolysis probes and Western blot), were used to corroborate the PPARG participation. 6IL effects on proliferation (measured by Trypan Blue exclusion) and apoptosis (phosphatidylserine identification by flow cytometer) were evaluated in conditions of chemical inhibition (GW9662) and silencing (RNA interference). A wound-healing assay was conducted on wild-type and stable PPARG-knockdown MCF-7 cells to evaluate the antimigrational effect of 6IL. Caspase-8 activity was evaluated to determine if the extrinsic pathway is involved in the effects of 6IL and I2 treatment.

resultsAntiproliferative and pro-apoptotic 6IL effects require the activation of PPARG. In addition, wound-healing assays show that 6IL is able to inhibit MCF-7 cell migration and that PPARG plays a role in this phenomenon. Finally, the data exclude the participation of the extrinsic apoptotic pathway in 6IL- and I2-induced apoptosis.

conclusionsThese results support the previously proposed mechanism, in which the I2 effects are mediated by 6IL, and they provide further support for the use of I2 as coadjuvant in breast cancer treatment.

Indexed as

ApoptosisArachidonic AcidCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansIodineMCF-7 CellsPPAR gammaWound HealingArachidonic AcidIodinePPAR gamma

Identifiers

PMID26376791
PMCPMC4573306
OpenAlexW1866062034

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.