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In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancer

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, July 2017
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Title
In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancer
Published in
Journal of Experimental & Clinical Cancer Research, July 2017
DOI 10.1186/s13046-017-0557-6
Pubmed ID
Authors

Megumi Fujita, Ai Hasegawa, Motohiro Yamamori, Noboru Okamura

Abstract

Troglitazone (TGZ) is a peroxisome proliferator-activated receptor gamma (PPARγ) agonist that has been investigated as a potential chemopreventive and chemotherapeutic agent. However, the antitumor efficacy and mechanisms of TGZ in pancreatic cancer have not been extensively investigated. This study was performed to investigate the in vitro and in vivo effects of TGZ against pancreatic cancer cell lines, as well as its action mechanisms in terms of PPARγ dependency and the Akt and mitogen-activated protein kinase (MAPK) pathways. We also evaluated the effects of TGZ on cell invasion and migration. MIA Paca2 and PANC-1 human pancreatic cancer cell lines were used. Cell viability and caspase-3 activity were detected using fluorescent reagents, and chromatin condensation was observed after staining the cells with Hoechst 33342. Protein expression levels were detected by western blot analysis. Invasion and migration assays were performed using 24-well chambers. The in vivo antitumor effects of TGZ were investigated in nude mice inoculated with MIA Paca2 cells. Mice were orally administered TGZ (200 mg/kg) every day for 5 weeks, and tumor volumes were measured bi-dimensionally. TGZ showed dose-dependent cytotoxicity against both cell lines, which was not attenuated by a PPARγ inhibitor. Further, TGZ induced chromatin condensation, elevated caspase-3 activity, and increased Bax/Bcl-2 relative expression in MIA Paca2 cells. TGZ also increased phosphorylation of Akt and MAPK (ERK/p38/JNK) in both cell lines, and a JNK inhibitor significantly increased the viability of MIA Paca2 cells. TGZ moderately inhibited cell migration. Tumor growth in the MIA Paca2 xenograft model was inhibited by TGZ administration, while mouse body weights in the treated group were not different from those of the vehicle administration group. We demonstrated for the first time the in vivo antitumor effects of TGZ in pancreatic cancer without marked adverse effects. TGZ induced mitochondria-mediated apoptosis in MIA Paca2 cells, and its cytotoxic effects were PPARγ-independent and occurred via the JNK pathway. Our results indicate that TGZ is a potential approach for the treatment of pancreatic cancer and warrants further studies regarding its detailed mechanisms and clinical efficacy.

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The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 14 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 21%
Student > Bachelor 2 14%
Student > Master 2 14%
Professor 2 14%
Other 1 7%
Other 3 21%
Unknown 1 7%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 29%
Pharmacology, Toxicology and Pharmaceutical Science 3 21%
Unspecified 1 7%
Psychology 1 7%
Medicine and Dentistry 1 7%
Other 1 7%
Unknown 3 21%

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 05 July 2017.
All research outputs
#10,141,840
of 11,430,110 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#425
of 606 outputs
Outputs of similar age
#217,971
of 259,783 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#5
of 9 outputs
Altmetric has tracked 11,430,110 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 606 research outputs from this source. They receive a mean Attention Score of 2.5. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 9 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.