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Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation

Interleukin-18 (IL-18), a proinflammatory cytokine, is produced by oral epithelia and carcinoma cells and implicated in tumor regression. Since its direct biological effect on oral cancer cells is not well defined, in this study, we employed a KB cell line to test IL-18 activity. Recombinant human I...

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Detalles Bibliográficos
Autores principales: Nilkaeo, Athip, Bhuvanath, Suthinee
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592604/
https://www.ncbi.nlm.nih.gov/pubmed/16951494
http://dx.doi.org/10.1155/MI/2006/67120
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author Nilkaeo, Athip
Bhuvanath, Suthinee
author_facet Nilkaeo, Athip
Bhuvanath, Suthinee
author_sort Nilkaeo, Athip
collection PubMed
description Interleukin-18 (IL-18), a proinflammatory cytokine, is produced by oral epithelia and carcinoma cells and implicated in tumor regression. Since its direct biological effect on oral cancer cells is not well defined, in this study, we employed a KB cell line to test IL-18 activity. Recombinant human IL-18 significantly inhibited KB cell proliferation in a dose-dependent fashion (P < .05) without increasing cytotoxicity. Analysis of its mode of action showed that IL-18 induced cell cycle arrest in the S phase; however, it did not trigger apoptotic cell death. Findings in this study indicate that the suppression of KB cell proliferation was attributed to the modulation of cell cycle progression, providing a new role of this cytokine in antitumor mechanisms.
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spelling pubmed-15926042006-10-23 Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation Nilkaeo, Athip Bhuvanath, Suthinee Mediators Inflamm Research Communication Interleukin-18 (IL-18), a proinflammatory cytokine, is produced by oral epithelia and carcinoma cells and implicated in tumor regression. Since its direct biological effect on oral cancer cells is not well defined, in this study, we employed a KB cell line to test IL-18 activity. Recombinant human IL-18 significantly inhibited KB cell proliferation in a dose-dependent fashion (P < .05) without increasing cytotoxicity. Analysis of its mode of action showed that IL-18 induced cell cycle arrest in the S phase; however, it did not trigger apoptotic cell death. Findings in this study indicate that the suppression of KB cell proliferation was attributed to the modulation of cell cycle progression, providing a new role of this cytokine in antitumor mechanisms. Hindawi Publishing Corporation 2006 2006-03-23 /pmc/articles/PMC1592604/ /pubmed/16951494 http://dx.doi.org/10.1155/MI/2006/67120 Text en Copyright © 2006 A. Nilkaeo and S. Bhuvanath. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Communication
Nilkaeo, Athip
Bhuvanath, Suthinee
Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title_full Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title_fullStr Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title_full_unstemmed Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title_short Role of Interleukin-18 in Modulation of Oral Carcinoma Cell Proliferation
title_sort role of interleukin-18 in modulation of oral carcinoma cell proliferation
topic Research Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592604/
https://www.ncbi.nlm.nih.gov/pubmed/16951494
http://dx.doi.org/10.1155/MI/2006/67120
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