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

Overview of attention for article published in Molecular Cancer, September 2015
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Title
Activation of peroxisome proliferator-activated receptor gamma is crucial for antitumoral effects of 6-iodolactone
Published in
Molecular Cancer, September 2015
DOI 10.1186/s12943-015-0436-8
Pubmed ID
Authors

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

Abstract

Molecular 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. The 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. Antiproliferative 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. These 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.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 53 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Mexico 2 4%
Unknown 51 96%

Demographic breakdown

Readers by professional status Count As %
Student > Master 7 13%
Student > Bachelor 7 13%
Researcher 6 11%
Student > Ph. D. Student 6 11%
Other 4 8%
Other 9 17%
Unknown 14 26%
Readers by discipline Count As %
Medicine and Dentistry 8 15%
Biochemistry, Genetics and Molecular Biology 8 15%
Agricultural and Biological Sciences 7 13%
Pharmacology, Toxicology and Pharmaceutical Science 4 8%
Immunology and Microbiology 3 6%
Other 8 15%
Unknown 15 28%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 June 2016.
All research outputs
#17,773,420
of 22,828,180 outputs
Outputs from Molecular Cancer
#1,203
of 1,721 outputs
Outputs of similar age
#183,338
of 272,396 outputs
Outputs of similar age from Molecular Cancer
#26
of 34 outputs
Altmetric has tracked 22,828,180 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,721 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 25th percentile – i.e., 25% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 272,396 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 34 others from the same source and published within six weeks on either side of this one. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.