Wound healing effects of new 15-hydroxyprostaglandin dehydrogenase inhibitors

Piao, Yu Lan; Wu, Ying; Seo, Seung Yong; Lim, Sung Chul; Cho, Hoon

doi:10.1016/j.plefa.2014.09.011

Cited by 9 publications

(9 citation statements)

References 32 publications

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“…Activation of PPARγ in lung cancer cell lines has induced differentiation and apoptosis . Additional recent studies provide further evidence demonstrating these agents may be useful in colon, neural, ovarian, melanoma, and lung cancer ; however, mechanisms of downstream action may vary between tissue types. In colon cancer, a principal finding of ciglitazone treatment was alterations in chaperones associated with protein folding .…”

Section: Introductionmentioning

confidence: 97%

Functional activation of PPARγ in human upper aerodigestive cancer cell lines

et al. 2016

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Upper aerodigestive cancer is an aggressive malignancy with relatively stagnant long-term survival rates over 20 yr. Recent studies have demonstrated that exploitation of PPARγ pathways may be a novel therapy for cancer and its prevention. We tested whether PPARγ is expressed and inducible in aerodigestive carcinoma cells and whether it is present in human upper aerodigestive tumors. Human oral cancer CA-9-22 and NA cell lines were treated with the PPAR activators eicosatetraynoic acid (ETYA), 15-deoxy-δ-12,14-prostaglandin J2 (PG-J2), and the thiazolidinedione, ciglitazone, and evaluated for their ability to functionally activate PPARγ luciferase reporter gene constructs. Cellular proliferation and clonogenic potential after PPARγ ligand treatment were also evaluated. Aerodigestive cancer specimens and normal tissues were evaluated for PPARγ expression on gene expression profiling and immunoblotting. Functional activation of PPARγ reporter gene constructs and increases in PPARγ protein were confirmed in the nuclear compartment after PPARγ ligand treatment. Significant decreases in cell proliferation and clonogenic potential resulted from treatment. Lipid accumulation was induced by PPARγ activator treatment. 75% of tumor specimens and 100% of normal control tissues expressed PPARγ RNA, and PPARγ protein was confirmed in 66% of tumor specimens analyzed by immunoblotting. We conclude PPARγ can be functionally activated in upper aerodigestive cancer and that its activation downregulates several features of the neoplastic phenotype. PPARγ expression in human upper aerodigestive tract tumors and normal cells potentially legitimizes it as a novel intervention target in this disease.

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Section: Introductionmentioning

confidence: 97%

Functional activation of PPARγ in human upper aerodigestive cancer cell lines

et al. 2016

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“…Previous research confirmed that the level of PGE 2 was much higher in the TD88 treatment group than in the control group [5,10].…”

Section: Molecular Biologic Analysismentioning

confidence: 75%

“…Animals were subjected to skin wounding as previously described [9,10]. The experiment involved 10 adult male guinea pigs (250-350 g) to identify the experimental effects more accurately by minimizing the hormonal effects.…”

Section: Manufacturing Animal Modelmentioning

confidence: 99%

Effect of 15-hydroxyprostaglandin dehydrogenase inhibitor on wound healing

Seo

Han

Bae

et al. 2015

Prostaglandins, Leukotrienes and Essential Fatty Acids

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“…23 It appears that the nature of the moiety linking through an ether linkage to the C4 position of benzylidene-2,4-thiazolidinedione plays an important role in determining the potency of inhibition. [24][25][26] The structures of these thiazolidinedione analogues are shown in Figure 1. Previously, our studies have also shown that the introduction of a chlorine atom at the C3 position of benzylidene-2,4-thiazolidinedione greatly increases inhibitory potency.…”

Section: Resultsmentioning

confidence: 99%