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NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells

Inflammatory and microenvironmental factors produced by cancer cells are thought to directly or indirectly promote cancer cell growth. Prostaglandins, including prostaglandin E2, have key roles as a microenvironment factor in influencing the development of tumors, and are produced by the rate limiti...

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Detalles Bibliográficos
Autores principales: Kitanaka, Nanako, Nakano, Rei, Kitanaka, Taku, Namba, Shinichi, Konno, Tadayoshi, Nakayama, Tomohiro, Sugiya, Hiroshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6298655/
https://www.ncbi.nlm.nih.gov/pubmed/30562372
http://dx.doi.org/10.1371/journal.pone.0208955
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author Kitanaka, Nanako
Nakano, Rei
Kitanaka, Taku
Namba, Shinichi
Konno, Tadayoshi
Nakayama, Tomohiro
Sugiya, Hiroshi
author_facet Kitanaka, Nanako
Nakano, Rei
Kitanaka, Taku
Namba, Shinichi
Konno, Tadayoshi
Nakayama, Tomohiro
Sugiya, Hiroshi
author_sort Kitanaka, Nanako
collection PubMed
description Inflammatory and microenvironmental factors produced by cancer cells are thought to directly or indirectly promote cancer cell growth. Prostaglandins, including prostaglandin E2, have key roles as a microenvironment factor in influencing the development of tumors, and are produced by the rate limiting enzyme cyclooxygenase 2 (COX-2). In this study, we used canine melanoma cells treated with the proinflammatory cytokine interleukin 1β (IL-1β) and investigated the transcriptional factor nuclear factor-κB (NF-κB) signaling in IL-1β-induced COX-2 expression. IL-1β induced prostaglandin E2 release and COX-2 mRNA expression in a time- and dose-dependent manner. In the cells treated with the NF-κB inhibitors BAY11-7082 and TPC-1, IL-1β-mediated prostaglandin E2 release and COX-2 mRNA expression were inhibited. IL-1β also provoked phosphorylation of p65/RelA and p105/NF-κB1, which are members of the NF-κB families. The IL-1β-induced phosphorylation of p65 and p105 was attenuated in the presence of both NF-κB inhibitors. In melanoma cells transfected with siRNA of p65 or p105, IL-1β-mediated COX-2 mRNA expression was inhibited. These findings suggest that canonical activation of NF-κB signaling plays a crucial role for inflammatory states in melanoma cells.
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spelling pubmed-62986552018-12-28 NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells Kitanaka, Nanako Nakano, Rei Kitanaka, Taku Namba, Shinichi Konno, Tadayoshi Nakayama, Tomohiro Sugiya, Hiroshi PLoS One Research Article Inflammatory and microenvironmental factors produced by cancer cells are thought to directly or indirectly promote cancer cell growth. Prostaglandins, including prostaglandin E2, have key roles as a microenvironment factor in influencing the development of tumors, and are produced by the rate limiting enzyme cyclooxygenase 2 (COX-2). In this study, we used canine melanoma cells treated with the proinflammatory cytokine interleukin 1β (IL-1β) and investigated the transcriptional factor nuclear factor-κB (NF-κB) signaling in IL-1β-induced COX-2 expression. IL-1β induced prostaglandin E2 release and COX-2 mRNA expression in a time- and dose-dependent manner. In the cells treated with the NF-κB inhibitors BAY11-7082 and TPC-1, IL-1β-mediated prostaglandin E2 release and COX-2 mRNA expression were inhibited. IL-1β also provoked phosphorylation of p65/RelA and p105/NF-κB1, which are members of the NF-κB families. The IL-1β-induced phosphorylation of p65 and p105 was attenuated in the presence of both NF-κB inhibitors. In melanoma cells transfected with siRNA of p65 or p105, IL-1β-mediated COX-2 mRNA expression was inhibited. These findings suggest that canonical activation of NF-κB signaling plays a crucial role for inflammatory states in melanoma cells. Public Library of Science 2018-12-18 /pmc/articles/PMC6298655/ /pubmed/30562372 http://dx.doi.org/10.1371/journal.pone.0208955 Text en © 2018 Kitanaka et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Kitanaka, Nanako
Nakano, Rei
Kitanaka, Taku
Namba, Shinichi
Konno, Tadayoshi
Nakayama, Tomohiro
Sugiya, Hiroshi
NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title_full NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title_fullStr NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title_full_unstemmed NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title_short NF-κB p65 and p105 implicate in interleukin 1β-mediated COX-2 expression in melanoma cells
title_sort nf-κb p65 and p105 implicate in interleukin 1β-mediated cox-2 expression in melanoma cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6298655/
https://www.ncbi.nlm.nih.gov/pubmed/30562372
http://dx.doi.org/10.1371/journal.pone.0208955
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