n-3 and n-6 Polyunsaturated fatty acids induce the expression of COX-2 via PPARγ activation in human keratinocyte HaCaT cells

Chene, Gerald; Dubourdeau, Marc; Balard, Patricia; Escoubet-Lozach, Laure; Orfila, C; Berry, Antoine; Bernad, José; Ariès, Marie-Françoise; Charvéron, M.; Pipy, Bernard

doi:10.1016/j.bbalip.2007.02.014

Cited by 49 publications

(42 citation statements)

References 72 publications

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“…A possible induction of COX-2 by PPAR-g as proposed by others (34) was not supported in view of an approximate concurrent upregulation of both mRNAs. Vice versa, a potential stimulatory action of COX-2 on PPAR-g was excluded by data showing that inhibition of COX-2 activity by NS-398 did not alter cannabidiol-induced PPAR-g expression within the 8-hour incubation period evaluated here.…”

Section: Discussionmentioning

confidence: 76%

COX-2 and PPAR-γ Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells

Ramer

Heinemann

Merkord

et al. 2013

Molecular Cancer Therapeutics

176

150

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The antitumorigenic mechanism of cannabidiol is still controversial. This study investigates the role of COX-2 and PPAR-g in cannabidiol's proapoptotic and tumor-regressive action. In lung cancer cell lines (A549, H460) and primary cells from a patient with lung cancer, cannabidiol elicited decreased viability associated with apoptosis. Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-g antagonist), and siRNA targeting COX-2 and PPAR-g. Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-g mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-g mRNA when compared with vehicle. In response to cannabidiol, tumor cell lines exhibited increased levels of COX-2-dependent prostaglandins (PG) among which PGD 2 and 15-deoxy-D 12,14 -PGJ 2 (15d-PGJ 2 ) caused a translocation of PPAR-g to the nucleus and induced a PPAR-g-dependent apoptotic cell death. Moreover, in A549-xenografted nude mice, cannabidiol caused upregulation of COX-2 and PPAR-g in tumor tissue and tumor regression that was reversible by GW9662. Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-g and a subsequent nuclear translocation of PPAR-g by COX-2-dependent PGs. Mol Cancer Ther; 12(1); 69-82. Ó2012 AACR.

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Section: Discussionmentioning

confidence: 76%

COX-2 and PPAR-γ Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells

Ramer

Heinemann

Merkord

et al. 2013

Molecular Cancer Therapeutics

176

150

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“…stimulation procedure . It has previously been shown that EPA induces COX-2, even in the absence of any stimulant, and that this induction is PPAR ␥ -mediated ( 57 ).…”

Section: Discussionmentioning

confidence: 95%

Evaluation of suppressive and pro-resolving effects of EPA and DHA in human primary monocytes and T-helper cells

Jaudszus

Gruen

Watzl

et al. 2013

Journal of Lipid Research

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“…A previous study demonstrated that COX-2 contains a PPRE in the promoter region and is a target for PPAR-mediated transactivation in epithelial cells 65 and immortalized keratinocytes 66 . Importantly, COX-2 induction has been implicated in UV-mediated processes ranging from carcinogenesis to local and systemic immunosuppression 29,30,[67][68][69] .…”

Section: Pparγ and Uvrmentioning

confidence: 99%

Oxidized glycerophosphocholines as biologically active mediators for ultraviolet radiation-mediated effects

Konger

Marathe

Yao

et al. 2008

Prostaglandins & Other Lipid Mediators

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Ultraviolet light radiation (UVR) has profound effects upon human skin. Yet, the exact targets for UVR are unclear. Inasmuch as UVR is a known pro-oxidative stressor, one potential target for UVR could be oxidatively modified glycerophosphocholines (GPC). Importantly, recent studies demonstrate that these oxidized GPCs (ox-GPC) are potent agonists for the platelet-activating factor receptor and peroxisome proliferator-activated receptor gamma. This review discusses these new biologically active lipids and their down-stream receptor targets that provide a unique system of biosensors for detecting and responding to UVR photo-oxidation.

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n-3 and n-6 Polyunsaturated fatty acids induce the expression of COX-2 via PPARγ activation in human keratinocyte HaCaT cells

Cited by 49 publications

References 72 publications

COX-2 and PPAR-γ Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells

COX-2 and PPAR-γ Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells

Evaluation of suppressive and pro-resolving effects of EPA and DHA in human primary monocytes and T-helper cells

Oxidized glycerophosphocholines as biologically active mediators for ultraviolet radiation-mediated effects

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